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1
Gao, Chun-Hui, Wen-Ping Wei, Hui-Ling Tao, Li-Kai Cai, Wan-Zhong Jia, Lihua Hu, and Min Yang. "Cross-talk between the three furA orthologs in Mycobacterium smegmatis and the contribution to isoniazid resistance." Journal of Biochemistry 166, no. 3 (April 16, 2019): 237–43. http://dx.doi.org/10.1093/jb/mvz030.
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Abstract The ferric uptake regulator A (FurA) plays an essential role in responding to oxidative stress in mycobacteria. The genome of Mycobacterium smegmatis harbours three FurA orthologs; however, the potential cross-talk and contribution to drug resistance of different furA operon remain underdetermined. In this study, we characterized the cross-regulation and effect in drug resistance of these orthologs from M. smegmatis. Cross-binding of FurA protein to furA promoter was observed. The binding of FurA1 to furA3p and FurA2 to furA1p or furA3p is even more pronounced than their self-binding. The three FurA proteins are all functional at repressing the expression of the peroxidase enzyme katG1/katG2 in vivo. When overexpressing any of the furA orthologs in M. smegmatis, the bacteria become more resistant to isoniazid (INH). This pattern is consistent with that in Mycobacterium bovis. However, the knockdown of furA does not affect the INH sensitivity. This is the first report of cross-talk and contribution to drug resistance of all three furA orthologs in M. smegmatis.
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Dubois, Christophe, Laurence Panicot-Dubois, Barbara C. Furie, and Bruce Furie. "Direct Real Time Visualization of Platelet Calclium Signaling In Vivo: Role of Platelet Activation and Thrombus Formation in a Living Mouse." Blood 104, no. 11 (November 16, 2004): 325. http://dx.doi.org/10.1182/blood.v104.11.325.325.
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Abstract Intracellular calcium mobilization plays a critical role in platelet signaling. Upon platelet activation, an intracellular calcium mobilization leads to the activation of various intracellular and membrane proteins, including integrins involved in both platelet shape change and aggregation. The goal of the present study was to monitor platelet calcium mobilization in vivo in an intact animal and to determine which intracellular pathways are dominant in platelet accumulation into the developing thrombus. Platelets were isolated from mice, washed, loaded with a calcium-sensitive fluorochrome, Fura2-AM and then infused into a recipient mouse. We studied Fura2-AM loaded platelet incorporation during arterial thrombus development following laser injury of the vessel wall in the cremaster microcirculation of living mice using high speed intravital widefield digital microscopy. Fura-2 loaded platelets were monitored by excitation at 380 nm; this fluorescence reports the basal calcium levels in platelets. Calcium mobilization was monitored by excitation at 340 nm where the fluorescence intensity reflects Fura2-calcium complex formation. We observed that platelets bind to the growing thrombus independent of calcium mobilization. However, the stable incorporation of platelets into the thrombus correlated with a significant intracellular calcium increase. Once the thrombus reached maximal size at about 100 seconds, the calcium mobilization also reached maximal intensity. Subsequently, platelets that did not mobilize calcium dissociated from the thrombus. We confirmed these observations by using platelets treated with the calcium chelators, BAPTA-AM or EGTA-AM. We observed a significant inhibition of platelet accumulation into the thrombus, indicating that the intracellular calcium increase is necessary in vivo for the stable accumulation of the platelets into the thrombus. We also evaluated the involvement in vivo of two platelet agonists, ADP and thromboxane A2 (TxA2), on calcium mobilization and platelet incorporation into thrombi. When platelets were treated with aspirin or with the P2Y1 antagonist A3P5P (adenosine 3′-phosphate-5′-phosphate), we observed a partial decrease in both calcium mobilization and platelet accumulation into the thrombus. These results indicate that TxA2 and ADP via the P2Y1 receptor are involved in vivo in platelet activation upon vessel wall injury in this thrombosis model. When platelets were treated with both compounds, we completely inhibited the calcium increase and the incorporation of platelets into the thrombus. Altogether, our results directly show, for the first time in vivo, the importance of the calcium mobilization on platelet accumulation into the developing thrombus. The platelet agonists TxA2 and ADP both play an important and complementary role on platelet activation by acting on the mobilization of the intracellular calcium.
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James-Kracke, M. R. "Calmodulin activation of the Ca2+ pump revealed by fluorescent chelator dyes in human red blood cell ghosts." Journal of General Physiology 99, no. 1 (January 1, 1992): 41–62. http://dx.doi.org/10.1085/jgp.99.1.41.
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Ca2+ transport in red blood cell ghosts was monitored with fura2 or quin2 incorporated as the free acid during resealing. This is the first report of active transport monitored by the fluorescent intensity of the chelator dyes fura2 (5-50 microM) or quin2 (250 microM) in hemoglobin-depleted ghosts. Since there are no intracellular compartments in ghosts and the intracellular concentrations of all assay chelator substances including calmodulin (CaM), the dyes, and ATP could be set, the intracellular concentrations of free and total Ca [( Cafree]i and [Catotal]i) could be calculated during the transport. Ghosts prepared with or without CaM rapidly extruded Ca2+ to a steady-state concentration of 60-100 nM. A 10(4)-fold gradient for Ca2+ was routinely produced in medium containing 1 mM Ca2+. During active Ca2+ extrusion, d[Cafree]i/dt was a second order function of [Cafree]i and was independent of the dye concentration, whereas d[Catotal]i/dt increased as a first order function of both the [Cafree]i and the concentration of the Ca:dye complex. CaM (5 microM) increased d[Catotal]i/dt by 400% at 1 microM [Cafree]i, while d[Cafree]i/dt increased by only 25%. From a series of experiments we conclude that chelated forms of Ca2+ serve as substrates for the pump under permissive control of the [Cafree]i, and this dual effect may explain cooperativity. Free Ca2+ is extruded, and probably also Ca2+ bound to CaM or other chelators, while CaM and the chelators are retained in the cell.
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Lee, Meng-Luen, Erna Sulistyowati, Jong-Hau Hsu, Bo-Yau Huang, Zen-Kong Dai, Bin-Nan Wu, Yu-Ying Chao, and Jwu-Lai Yeh. "KMUP-1 Ameliorates Ischemia-Induced Cardiomyocyte Apoptosis through the NO–cGMP–MAPK Signaling Pathways." Molecules 24, no. 7 (April 8, 2019): 1376. http://dx.doi.org/10.3390/molecules24071376.
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To test whether KMUP-1 (7-[2-[4-(2-chlorophenyl) piperazinyl]ethyl]-1,3-dimethylxanthine) prevents myocardial ischemia-induced apoptosis, we examined KMUP-1-treated H9c2 cells culture. Recent attention has focused on the activation of nitric oxide (NO)-guanosine 3', 5'cyclic monophosphate (cGMP)-protein kinase G (PKG) signaling pathway triggered by mitogen-activated protein kinase (MAPK) family, including extracellular-signal regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 in the mechanism of cardiac protection during ischemia-induced cell-death. We propose that KMUP-1 inhibits ischemia-induced apoptosis in H9c2 cells culture through these pathways. Cell viability was assessed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and apoptotic evaluation was conducted using DNA ladder assay and Hoechst 33342 staining. The level of intracellular calcium was detected using - Fura2-acetoxymethyl (Fura2-AM) staining, and mitochondrial calcium with Rhod 2-acetoxymethyl (Rhod 2-AM) staining under fluorescence microscopic observation. The expression of endothelium NO synthase (eNOS), inducible NO synthase (iNOS), soluble guanylate cyclase α1 (sGCα1), PKG, Bcl-2/Bax ratio, ERK1/2, p38, and JNK proteins were measured by Western blotting assay. KMUP-1 pretreatment improved cell viability and inhibited ischemia-induced apoptosis of H9c2 cells. Calcium overload both in the intracellular and mitochondrial sites was attenuated by KMUP-1 pretreatment. Moreover, KMUP-1 reduced intracellular reactive oxygen species (ROS), increased plasma NOx (nitrite and nitrate) level, and the expression of eNOS. Otherwise, the iNOS expression was downregulated. KMUP-1 pretreatment upregulated the expression of sGCα1 and PKG protein. The ratio of Bcl-2/Bax expression was increased by the elevated level of Bcl2 and decreased level of Bax. In comparison with the ischemia group, KMUP-1 pretreatment groups reduced the expression of phosphorylated extracellular signal-regulated kinases ERK1/2, p-p38, and p-JNK as well. Therefore, KMUP-1 inhibits myocardial ischemia-induced apoptosis by restoration of cellular calcium influx through the mechanism of NO-cGMP-MAPK pathways.
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Sago, Haruhiko, and Kazuso linuma. "Cell Shape Change and Cytosolic Ca2+ in Human Umbilical-Vein Endothelial Cells Stimulated with Thrombin." Thrombosis and Haemostasis 67, no. 03 (1992): 331–34. http://dx.doi.org/10.1055/s-0038-1648442.
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SummaryWe quantified thrombin-induced endothelial cells shape change and investigated the role of Ca2+ in such shape change. We used the fluorescent Ca2+ indicator, fura2, to measure both shape change as cell size and intracellular free Ca2+ ([Ca2+]i), in cultured human umbilical-vein endothelial cells (HUVEC). Thrombin induced concentration-dependent decreases in cell size (percentage of cell size at 6 min after stimulation with 0.01 U/ml, 0.1 U/ml, or 1 U/ml thrombin) was 90.1 ± 1.5%, 78.1 ± 2.4%, and 40.9 ± 2.4%, respectively. Thrombin also increased [Ca2+]i in a concentration-dependent manner. Both depletion of extracellular Ca2+, and also the addition of W5, a calmodulin antagonist, inhibited thrombin-induced size reduction. These results indicate an association between shape change and [Ca2+]i mobilization in human endothelial cells stimulated by thrombin.
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Morita, Mitsuhiro, Jinichi Susuki, Takanori Moto, Chitose Higuchi, and Yoshihisa Kudo. "A Novel Method to Quantify Calcium Response Pattern and Oscillation Using Fura2 and Acridine Orange." Journal of Pharmacological Sciences 94, no. 1 (2004): 25–30. http://dx.doi.org/10.1254/jphs.94.25.
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Schafer, AI, GB Zavoico, J. Loscalzo, and AK Maas. "Synergistic inhibition of platelet activation by plasmin and prostaglandin I2." Blood 69, no. 5 (May 1, 1987): 1504–7. http://dx.doi.org/10.1182/blood.v69.5.1504.1504.
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Abstract Endothelial cell prostacyclin (PGI2) inhibits platelet activation by raising platelet cyclic AMP. Previously, platelet activation was also shown to be blocked by plasmin formed by endothelium-derived tissue plasminogen activator (TPA). We have now studied interactions between PGI2 and plasmin in the control of platelet function. PGI2 and plasmin cause synergistic inhibition of thrombin- and ADP-induced aggregation of washed platelets. Inhibition by PGI2 is similarly potentiated by TPA added to platelet-rich plasma to generate plasmin. Thrombin-stimulated rise in platelet cytosolic Ca2+, measured by fura2 fluorescence, and thromboxane A2 formation, measured by radioimmunoassay (RIA), are likewise synergistically inhibited by PGI2 and plasmin. Plasmin neither increases nor potentiates PGI2-stimulated increases in platelet cyclic AMP. Thus, PGI2 and plasmin cause synergistic inhibition of platelet activation by both cyclic AMP-dependent and independent mechanisms. This interaction between two different endothelium-derived products may play an important role in localizing the hemostatic plug to a site of vascular injury by preventing further thrombin-mediated accrual of platelets.
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Schafer, AI, GB Zavoico, J. Loscalzo, and AK Maas. "Synergistic inhibition of platelet activation by plasmin and prostaglandin I2." Blood 69, no. 5 (May 1, 1987): 1504–7. http://dx.doi.org/10.1182/blood.v69.5.1504.bloodjournal6951504.
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Endothelial cell prostacyclin (PGI2) inhibits platelet activation by raising platelet cyclic AMP. Previously, platelet activation was also shown to be blocked by plasmin formed by endothelium-derived tissue plasminogen activator (TPA). We have now studied interactions between PGI2 and plasmin in the control of platelet function. PGI2 and plasmin cause synergistic inhibition of thrombin- and ADP-induced aggregation of washed platelets. Inhibition by PGI2 is similarly potentiated by TPA added to platelet-rich plasma to generate plasmin. Thrombin-stimulated rise in platelet cytosolic Ca2+, measured by fura2 fluorescence, and thromboxane A2 formation, measured by radioimmunoassay (RIA), are likewise synergistically inhibited by PGI2 and plasmin. Plasmin neither increases nor potentiates PGI2-stimulated increases in platelet cyclic AMP. Thus, PGI2 and plasmin cause synergistic inhibition of platelet activation by both cyclic AMP-dependent and independent mechanisms. This interaction between two different endothelium-derived products may play an important role in localizing the hemostatic plug to a site of vascular injury by preventing further thrombin-mediated accrual of platelets.
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Li, Shu, Jingyi Xue, Zhipeng Sun, Tiantian Liu, Lane Zhang, Limin Wang, Hongjie You, Zheng Fan, Yuanyuan Zheng, and Dali Luo. "CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction with Orai1." Cellular Physiology and Biochemistry 46, no. 3 (2018): 1042–54. http://dx.doi.org/10.1159/000488835.
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Background/Aims: Upon Ca2+ store depletion, stromal interaction molecule 1 (STIM1) oligomerizes, redistributes near plasmalemma to interact with Ca2+ selective channel-forming subunit (Orai1) and initiates store-operated Ca2+ entry (SOCE). Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a regulator of SOCE, but how CaMKII regulates SOCE remains obscure. Methods: Using Fura2, confocal microscopy, co-immunoprecipitation, specific blocker and overexpression/knockdown approaches, we evaluated STIM1 aggregation and its interaction with Orai1, and SOCE upon Ca2+ store depletion in thapsigargin (TG) treated HEK293 and HeLa cells. Results: Overexpression of CaMKIIδ enhanced TG-induced STIM1 co-localization and interaction with Orai1 as well as SOCE. In contrast, CaMKIIδ knockdown and a specific inhibitor of CaMKII suppressed them. In addition, overexpression or knockdown of CaMKIIδ in TG treated cells exhibited increased or reduced STIM1 clustering and plasmalemma redistribution, respectively. Conclusion: CaMKII up-regulates SOCE by increasing STIM1 aggregation and interaction with Orai1. This study provides an additional insight into SOCE regulation and a potential mechanism for CaMKII involvement in some pathological situations through crosstalk with SOCE.
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Marchetti, C., C. Amico, and C. Usai. "Functional characterization of the effect of nimodipine on the calcium current in rat cerebellar granule cells." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 1169–80. http://dx.doi.org/10.1152/jn.1995.73.3.1169.
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1. We investigated the effect of nimodipine on the calcium current in dissociated cerebellar granule cells from 8-day-old rats. We measured the whole cell current and the depolarization-induced internal calcium elevation in Fura2-loaded cells exposed to high-potassium solutions. 2. Nimodipine maximally depressed the peak calcium current from holding potential (Vh) = -80 mV by 25% and the inactivation resistant residual current from Vh = -50 mV by 44%. The nimodipine-sensitive current had the same amplitude under both conditions and the half-maximal inhibition concentration (IC50) was close to 50 nM. 3. In contrast to other components of the calcium current, the nimodipine-sensitive current did not inactivate significantly during 1-s depolarization and it was weakly sensitive to the holding potential and to depolarizing conditioning prepulses. The effect of nimodipine was higher on the current elicited by small depolarizations and the current at -30 mV was depressed by < or = 70%. Depolarizing prepulses enhanced the effect of 1 nM (but not that of 1 microM) nimodipine. 4. In Fura2-loaded cells, nimodipine strongly antagonized the internal calcium rise due to superfusion with 15-75 mM potassium. The effect was significantly more potent on the internal calcium rise determined by lower depolarizations, with 80% inhibition of the peak response to 25 mM KCl. The dose dependence of this depression was best approximated by a two-site curve with IC50(1) = 0.27 nM and IC50(2) = 65 nM. The time course of recovery was dependent on the duration of treatment, suggesting a close interaction between nimodipine and the lipid membrane. 5. The effect of 1 microM nimodipine was not influenced by predepolarizations determined by treatments with calcium-free elevated potassium solutions, but when doses as low as 1 nM were applied the fast decay of the calcium level suggested a voltage dependence of the effect. Nimodipine also depressed < or = 90% of the plateau phase of the depolarization-induced internal calcium rise at different depolarizations. 6. Incubation in omega-conotoxin, fraction GVIA (5 microM) did not cause any significant decrease in the calcium response, whereas omega-agatoxin, fraction IVA (0.5 microM) depressed the calcium peak by 40-60% and its effect was additive with that of nimodipine. 7. We conclude that the nimodipine-sensitive current is a persistent, inactivation-resistant current that activates at a membrane potential lower than the other components and is likely to be responsible for the elevation of calcium determined by nonovershooting, prolonged depolarizations in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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Edelfors, S., and A. Ravn-Jonsen. "Structure-activity relationships in the effect of organic solvents on the nerve cell determined by the synaptosomal leakage of FURA2." Toxicology Letters 88 (October 1996): 25. http://dx.doi.org/10.1016/s0378-4274(96)80090-7.
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Forbes, John R., and Philippe Gros. "Iron, manganese, and cobalt transport by Nramp1 (Slc11a1) and Nramp2 (Slc11a2) expressed at the plasma membrane." Blood 102, no. 5 (September 1, 2003): 1884–92. http://dx.doi.org/10.1182/blood-2003-02-0425.
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AbstractMutations in the Nramp1 gene (Slc11a1) cause susceptibility to infection by intracellular pathogens. The Nramp1 protein is expressed at the phagosomal membrane of macrophages and neutrophils and is a paralog of the Nramp2 (Slc11a2) iron transporter. The Nramp1 transport mechanism at the phagosomal membrane has remained controversial. An Nramp1 protein modified by insertion of a hemagglutinin epitope into the predicted TM7/8 loop was expressed at the plasma membrane of Chinese hamster ovary cells as demonstrated by immunofluorescence and surface biotinylation. Experiments in Nramp1HA transfectants using the metal-sensitive fluorophors calcein and Fura2 showed that Nramp1HA can mediate Fe2+, Mn2+, and Co2+ uptake. Similar results were obtained in transport studies using radioisotopic 55Fe2+ and 54Mn2+. Nramp1HA transport was dependent on time, temperature, and acidic pH, occurring down the proton gradient. These experiments suggest that Nramp1HA may be a more efficient transporter of Mn2+ compared to Fe2+ and a more efficient Mn2+ transporter than Nramp2HA. The membrane topology and transport properties of Nramp1HA and Nramp2HA were indistinguishable, suggesting that Nramp1 divalent-metal transport at the phagosomal membrane is mechanistically similar to that of Nramp2 at the membrane of acidified endosomes. These results clarify the mechanism by which Nramp1 contributes to phagocyte defenses against infections.
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O'Sullivan, A. J., and R. D. Burgoyne. "A comparison of bradykinin, angiotensin II and muscarinic stimulation of cultured bovine adrenal chromaffin cells." Bioscience Reports 9, no. 2 (April 1, 1989): 243–52. http://dx.doi.org/10.1007/bf01116001.
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Bradykinin, angiotensin II and a mascarnic agonist, acetyl-B-methacholine (methacholine) were all found to elict catecholamine release from cultured bovine adrenal chromaffin cells. Bradykinin was the most potent of these secretagogues and methacholine the weakest, with angiotenin II intermediate in efficacy. All three secretagogues were much less effective than nicotinic stimulation. The three secretagogues all produced a rise in cytoplasmic free calcium concentration ([Ca2+]i), measured with the fluorescent indicator fura2, which was partially independent of external calcium. In the case of bradykinin the full rise in ([Ca2+]i) may involve a component of calcium entry in addition to release of calcium from an internal store. Secretion was also found to be partially independent of external calcium. The different efficacies of the three secretagogues in elicting secretion were correlated with the rise in ([Ca2+]i) produced. The differeing efficacies of the three secretagogues may be due to the extent of release of calcium from an intracellular store which itself is less effective in eliciting secretion than a rise in [Ca2+]i following calcium entry due to nicotine. Bradykinin also stimulates calcium entry, and this may increase the efficacy of the initial rise in [Ca2+]i. Treatment with pertussis toxin resulted in an enhancement of secretion in response to all of the secretagogues.
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Durante, W., MH Kroll, PM Vanhoutte, and AI Schafer. "Endothelium-derived relaxing factor inhibits thrombin-induced platelet aggregation by inhibiting platelet phospholipase C." Blood 79, no. 1 (January 1, 1992): 110–16. http://dx.doi.org/10.1182/blood.v79.1.110.110.
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Abstract Endothelium-derived relaxing factor (EDRF) inhibits platelet function, but the mechanism underlying this inhibitory effect is not known. To examine this, cultured acetylsalicylic acid (ASA)-treated endothelial cells (EC) from bovine aorta (BAEC) or from human umbilical vein (HUVEC) were incubated with washed, ASA-treated human platelets. Incubation of platelets with either BAEC or HUVEC resulted in inhibition of thrombin-induced platelet aggregation that was dependent on the number of EC added. This effect was potentiated by superoxide dismutase and reversed by treating EC with NG-nitro-L-arginine or by treating platelets with methylene blue, indicating that the inhibition of platelet aggregation was due to the release of EDRF by EC. EC significantly blocked the thrombin stimulated breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the production of phosphatidic acid in [32P]orthophosphate-labeled platelets and of inositol trisphosphate in [3H]myoinositol-labeled platelets. In addition, the thrombin-mediated activation of protein kinase C (PKC) and phosphorylation of myosin light chain were inhibited in the presence of EC. Finally, thrombin stimulated an increase in cytosolic ionized calcium concentration ([Ca2+]i) in fura2-loaded platelets that was abolished by concentrations of EC which also blocked thrombin- induced aggregation. These data indicate that EDRF blocks thrombin- induced platelet aggregation by inhibiting the activation of PIP2- specific phospholipase C and thereby suppressing the consequent activation of PKC and the mobilization of [Ca2+]i.
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Durante, W., MH Kroll, PM Vanhoutte, and AI Schafer. "Endothelium-derived relaxing factor inhibits thrombin-induced platelet aggregation by inhibiting platelet phospholipase C." Blood 79, no. 1 (January 1, 1992): 110–16. http://dx.doi.org/10.1182/blood.v79.1.110.bloodjournal791110.
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Endothelium-derived relaxing factor (EDRF) inhibits platelet function, but the mechanism underlying this inhibitory effect is not known. To examine this, cultured acetylsalicylic acid (ASA)-treated endothelial cells (EC) from bovine aorta (BAEC) or from human umbilical vein (HUVEC) were incubated with washed, ASA-treated human platelets. Incubation of platelets with either BAEC or HUVEC resulted in inhibition of thrombin-induced platelet aggregation that was dependent on the number of EC added. This effect was potentiated by superoxide dismutase and reversed by treating EC with NG-nitro-L-arginine or by treating platelets with methylene blue, indicating that the inhibition of platelet aggregation was due to the release of EDRF by EC. EC significantly blocked the thrombin stimulated breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the production of phosphatidic acid in [32P]orthophosphate-labeled platelets and of inositol trisphosphate in [3H]myoinositol-labeled platelets. In addition, the thrombin-mediated activation of protein kinase C (PKC) and phosphorylation of myosin light chain were inhibited in the presence of EC. Finally, thrombin stimulated an increase in cytosolic ionized calcium concentration ([Ca2+]i) in fura2-loaded platelets that was abolished by concentrations of EC which also blocked thrombin- induced aggregation. These data indicate that EDRF blocks thrombin- induced platelet aggregation by inhibiting the activation of PIP2- specific phospholipase C and thereby suppressing the consequent activation of PKC and the mobilization of [Ca2+]i.
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Zhang, Lane, Limin Wang, Shu Li, Jingyi Xue, and Dali Luo. "Calsequestrin-1 Regulates Store-Operated Ca2+ Entry by Inhibiting STIM1 Aggregation." Cellular Physiology and Biochemistry 38, no. 6 (2016): 2183–93. http://dx.doi.org/10.1159/000445574.
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Background/Aims: Stromal interacting molecule-1 (STIM1) aggregation and redistribution to plasma membrane to interact with Orai1 constitute the core mechanism of store-operated Ca2+ entry (SOCE). Previous study has revealed that calsequestrin-1 (CSQ1) regulates SOCE in HEK293 cells through interacting with STIM1 and inhibiting STIM1/Orai1 interaction. Here, we further investigate how CSQ1/STIM1 interaction affects SOCE. Methods: Using confocal microscopy, STIM1 aggregation and co-localizations with CSQ1 or Orai1 upon Ca2+ store depletion by thapsigargin were measured and quantified by Imaris software in HeLa cells transfected with different CSQ1 mutants. The interactions of CSQ1/STIM1 and STIM1/Orai1, and internal Ca2+ changes were detected by co-immunoprecipitation and Fura2, respectively. Results: Wt-CSQ1 overexpression significantly reduced STIM1 clustering in the perimembrane and cytosolic regions, whereas over-expression of a C-terminal amino acid 362-396 deletion mutant (C35) did not. Consistently, a significant depression of SOCE, increased CSQ1 monomerization and CSQ1/STIM1 interaction, and a reduced STIM1/Orai1 association were observed in wt-CSQ1 but not in C35-transfected cells. Additionally, mutant lacking C-terminal AA 388-396 deletion exerted weaker potency in inhibiting STIM1 aggregation and association with Orai1 than wt-CSQ1. Conclusions: Our results demonstrate that CSQ1 monomers suppress SOCE by interacting with STIM1 and attenuating STIM1 aggregation via its C-terminal amino acid 362-396.
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Winston, F. K., L. E. Thibault, and E. J. Macarak. "An Analysis of the Time-Dependent Changes in Intracellular Calcium Concentration in Endothelial Cells in Culture Induced by Mechanical Stimulation." Journal of Biomechanical Engineering 115, no. 2 (May 1, 1993): 160–68. http://dx.doi.org/10.1115/1.2894116.
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When bovine pulmonary artery endothelial cells in culture are subjected to mechanical strain, their physiology is altered. Experimentally, this mechanical strain is generated by increased tension in the substrate to which the cells are attached and results in altered levels of fibronectin. Studies of the structural response of the endothelial cell suggest that this stimulus is transmitted to the cell membrane, organelles, and cytoskeleton by natural cell attachments in a quantifiable and predictable manner. This report examines altered intracellular calcium homeostasis as a possible messenger for the observed strain-induced physiologic response. In particular, using the intracellularly trapped calcium indicator dyes, Quin2 and Fura2, we observed changes in cytosolic free calcium ion concentration in response to biaxial strain of bovine pulmonary artery endothelial cells in culture. The magnitude and time course of this calcium transient resemble that produced by treatment with the calcium ionophore, Ionomycin, indicating that mechanical stimulation may alter cell membrane permeability to calcium. Additional experiments in the presence of EDTA indicated that calcium was also released from intracellular stores in response to strain. In order to explain the stretch-induced calcium transients, a first-order species conservation model is presented that takes into account both the cell’s structural response and the calcium homeostatic mechanisms of the cell. It is hypothesized that the cell’s calcium sequestering and pumping capabilities balanced with its mechanically induced changes in calcium ion permeability will determine the level and time course of calcium accumulation in the cytosol.
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Tolhurst, Gwen, Yue Zheng, Helen E. Parker, Abdella M. Habib, Frank Reimann, and Fiona M. Gribble. "Glutamine Triggers and Potentiates Glucagon-Like Peptide-1 Secretion by Raising Cytosolic Ca2+ and cAMP." Endocrinology 152, no. 2 (February 1, 2011): 405–13. http://dx.doi.org/10.1210/en.2010-0956.
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Abstract L-glutamine stimulates glucagon-like peptide 1 (GLP-1) secretion in human subjects and cell lines. As recent advances have enabled the study of primary GLP-1–releasing L cells, this study aimed to characterize glutamine-sensing pathways in native murine L cells. L cells were identified using transgenic mice with cell-specific expression of fluorescent markers. Cells were studied in primary colonic cultures from adult mice, or purified by flow cytometry for expression analysis. Intracellular Ca2+ was monitored in cultures loaded with Fura2, and cAMP was studied using Förster resonance energy transfer sensors expressed in GLUTag cells. Asparagine, phenylalanine, and glutamine (10 mm) triggered GLP-1 release from primary cultures, but glutamine was the most efficacious, increasing secretion 1.9-fold with an EC50 of 0.19 mm. Several amino acids triggered Ca2+ changes in L cells, comparable in magnitude to that induced by glutamine. Glutamine-induced Ca2+ responses were abolished in low Na+ solution and attenuated in Ca2+ free solution, suggesting a role for Na+ dependent uptake and Ca2+ influx. The greater effectiveness of glutamine as a secretagogue was paralleled by its ability to increase cAMP in GLUTag cells. Glutamine elevated intracellular cAMP to 36% of that produced by a maximal stimulus, whereas asparagine only increased intracellular cAMP by 24% and phenylalanine was without effect. Glutamine elevates both cytosolic Ca2+ and cAMP in L cells, which may account for the effectiveness of glutamine as a GLP-1 secretagogue. Therapeutic agents like glutamine that target synergistic pathways in L cells might play a future role in the treatment of type 2 diabetes.
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Tan, Ju Jing, Francis Boudreault, Damien Adam, Emmanuelle Brochiero, and Ryszard Grygorczyk. "Type 2 secretory cells are primary source of ATP release in mechanically stretched lung alveolar cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L49—L58. http://dx.doi.org/10.1152/ajplung.00321.2019.
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Extracellular ATP and its metabolites are potent paracrine modulators of lung alveolar cell function, including surfactant secretion and fluid transport, but the sources and mechanism of intra-alveolar ATP release remain unclear. To determine the contribution of gas-exchanging alveolar type 1 (AT1) and surfactant-secreting type 2 (AT2) cells to stretch-induced ATP release, we used quantitative real-time luminescence ATP imaging and rat primary alveolar cells cultured on silicon substrate for 2–7 days. When cultured on solid support, primary AT2 cells progressively transdifferentiated into AT1-like cells with ~20% of cells showing AT1 phenotype by day 2–3 (AT2:AT1 ≈ 4:1), while on day 7, the AT2:AT1 cell ratio was reversed with up to 80% of the cells displaying characteristics of AT1 cells. Stretch (1 s, 5–35%) induced ATP release from AT2/AT1 cell cultures, and it was highest on days 2 and 3 but declined in older cultures. ATP release tightly correlated with the number of remaining AT2 cells in culture, consistent with ~10-fold lower ATP release by AT1 than AT2 cells. ATP release was unaffected by inhibitors of putative ATP channels carbenoxolone and probenecid but was significantly diminished in cells loaded with calcium chelator BAPTA. These pharmacological modulators had similar effects on stretch-induced intracellular Ca2+ responses measured by Fura2 fluorescence. The study revealed that AT2 cells are the primary source of stretch-induced ATP release in heterocellular AT2/AT1 cell cultures, suggesting similar contribution in intact alveoli. Our results support a role for calcium-regulated mechanism but not ATP-conducting channels in ATP release by alveolar epithelial cells.
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Combettes, L., D. Tran, T. Tordjmann, M. Laurent, B. Berthon, and M. Claret. "Ca2+-mobilizing hormones induce sequentially ordered Ca2+ signals in multicellular systems of rat hepatocytes." Biochemical Journal 304, no. 2 (December 1, 1994): 585–94. http://dx.doi.org/10.1042/bj3040585.
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The development of hormone-mediated Ca2+ signals was analysed in polarized doublets, triplets and quadruplets of rat hepatocytes by video imaging of fura2 fluorescence. These multicellular models showed dilated bile canaliculi, and gap junctions were observed by using an anti-connexin-32 antibody. They also showed highly organized Ca2+ signals in response to vasopressin or noradrenaline. Surprisingly, the primary rises in intracellular Ca2+ concentration ([Ca2+]i) did not start randomly from any cell of the multiplet. It originated invariably in the same hepatocyte (first-responding cell), and then was propagated in a sequential manner to the nearest connected cells (cell 2, then 3, in triplets; cell 2, 3, then 4 in quadruplets). The sequential activation of the cells appeared to be an intrinsic property of multiplets of rat hepatocytes. (1) In the continued presence of hormones, the same sequential order was observed up to six times, i.e. at each train of oscillations occurring between the cells. (2) The order of [Ca2+]i responses was modified neither by the repeated addition of hormones nor by the hormonal dose. (3) The mechanical disruption of an intermediate cell slowed down the speed of the propagation, suggesting a role of gap junctions in the rapidity of the sequential activation of cells. (4) The same multiplet could have a different first-responding cell for vasopressin or noradrenaline, suggesting a role of the hormonal receptors in the sequentiality of cell responses. It is postulated that a functional heterogeneity of hormonal receptors, and the presence of functional gap junctions, are involved in the existence of sequentially ordered hormone-mediated [Ca2+]i rises in the multiplets of rat hepatocytes.
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Gekle, Michael, and Sigrid Mildenberger. "Glomerular Mesangial Cell pH Homeostasis Mediates Mineralocorticoid Receptor-Induced Cell Proliferation." Biomedicines 9, no. 9 (August 30, 2021): 1117. http://dx.doi.org/10.3390/biomedicines9091117.
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Mineralocorticoids (e.g., aldosterone) support chronic inflammatory tissue damage, including glomerular mesangial injury leading to glomerulosclerosis. Furthermore, aldosterone leads to activation of the extracellular signal-regulated kinases (ERK1/2) in rat glomerular mesangial cells (GMC). Because ERK1/2 can affect cellular pH homeostasis via activation of Na+/H+-exchange (NHE) and the resulting cellular alkalinization may support proliferation, we tested the hypothesis that aldosterone affects pH homeostasis and thereby cell proliferation as well as collagen secretion also in primary rat GMC. Cytoplasmic pH and calcium were assessed by single-cell fluorescence ratio imaging, using the dyes BCECF or FURA2, respectively. Proliferation was determined by cell counting, thymidine incorporation and collagen secretion by collagenase-sensitive proline incorporation and ERK1/2-phosphorylation by Western blot. Nanomolar aldosterone induces a rapid cytosolic alkalinization which is prevented by NHE inhibition (10 µmol/L EIPA) and by blockade of the mineralocorticoid receptor (100 nmol/L spironolactone). pH changes were not affected by inhibition of HCO3− transporters and were not dependent on HCO3−. Aldosterone enhanced ERK1/2 phosphorylation and inhibition of ERK1/2-phosphorylation (10 µmol/L U0126) prevented aldosterone-induced alkalinization. Furthermore, aldosterone induced proliferation of GMC and collagen secretion, both of which were prevented by U0126 and EIPA. Cytosolic calcium was not involved in this aldosterone action. In conclusion, our data show that aldosterone can induce GMC proliferation via a MR and ERK1/2-mediated activation of NHE with subsequent cytosolic alkalinization. GMC proliferation leads to glomerular hypercellularity and dysfunction. This effect presents a possible mechanism contributing to mineralocorticoid receptor-induced pathogenesis of glomerular mesangial injury during chronic kidney disease.
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Young, Coleman H., Bryce Snow, Stanley B. DeVore, Adithya Mohandass, Venkatesh V. Nemmara, Paul R. Thompson, Baskaran Thyagarajan, Amy M. Navratil, and Brian D. Cherrington. "Progesterone stimulates histone citrullination to increase IGFBP1 expression in uterine cells." Reproduction 162, no. 2 (August 1, 2021): 117–27. http://dx.doi.org/10.1530/rep-21-0132.
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Peptidylarginine deiminases (PAD) enzymes were initially characterized in uteri, but since then little research has examined their function in this tissue. PADs post-translationally convert arginine residues in target proteins to citrulline and are highly expressed in ovine caruncle epithelia and ovine uterine luminal epithelial (OLE)-derived cell line. Progesterone (P4) not only maintains the uterine epithelia but also regulates the expression of endometrial genes that code for proteins that comprise the histotroph and are critical during early pregnancy. Given this, we tested whether P4 stimulates PAD-catalyzed histone citrullination to epigenetically regulate expression of the histotroph gene insulin-like growth factor binding protein 1 (IGFBP1) in OLE cells. 100 nM P4 significantly increases IGFBP1 mRNA expression; however, this increase is attenuated by pre-treating OLE cells with 100 nM progesterone receptor antagonist RU486 or 2 µM of a pan-PAD inhibitor. P4 treatment of OLE cells also stimulates citrullination of histone H3 arginine residues 2, 8, and 17 leading to enrichment of the ovine IGFBP1 gene promoter. Since PAD2 nuclear translocation and catalytic activity require calcium, we next investigated whether P4 triggers calcium influx in OLE cells. OLE cells were pre-treated with 10 nM nicardipine, an L-type calcium channel blocker, followed by stimulation with P4. Using fura2-AM imaging, we found that P4 initiates a rapid calcium influx through L-type calcium channels in OLE cells. Furthermore, this influx is necessary for PAD2 nuclear translocation and resulting citrullination of histone H3 arginine residues 2, 8, and 17. Our work suggests that P4 stimulates rapid calcium influx through L-type calcium channels initiating PAD-catalyzed histone citrullination and an increase in IGFBP1 expression.
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Siffert, W., G. Siffert, P. Scheid, and J. W. N. Akkerman. "Activation of Na+/H+ exchange and Ca2+ mobilization start simultaneously in thrombin-stimulated platelets. Evidence that platelet shape change disturbs early rises of BCECF fluorescence which causes an underestimation of actual cytosolic alkalinization." Biochemical Journal 258, no. 2 (March 1, 1989): 521–27. http://dx.doi.org/10.1042/bj2580521.
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Although an increase in cytosolic pH (pHi) caused by Na+/H+ exchange enhances Ca2+ mobilization in platelets stimulated by low concentrations of thrombin [Siffert & Akkerman (1987) Nature (London) 325, 456-458], studies using fluorescent indicators for pHi (BCECF) and [Ca2+]i (fura2) suggest that Ca2+ is mobilized while the cytosolic pH decreases. Several lines of evidence indicate that the initial fall in BCECF fluorescence is not due to cytosolic acidification but is caused by a platelet shape change. (1) Pulse stimulation of platelets by successive addition of hirudin (4 unit/ml) and thrombin (0.2 unit/ml) induced a shape change of 43 +/- 8% and a fall in BCECF fluorescence, which both remained unchanged when Na+/H+ exchange was inhibited by ethylisopropylamiloride (EIPA, 100 microM). (2) Increasing the thrombin concentration to 0.4 unit/ml doubled the shape change and the fall in BCECF fluorescence, but again EIPA had no effect on these responses. (3) Treating platelets with 2 microM-ADP induced shape change and a decline in BCECF fluorescence that was unaffected by EIPA. (4) A second addition of thrombin to platelets that had already undergone shape change induced an immediate increase in BCECF fluorescence without a prior decrease. (5) Activation of protein kinase C by 1,2-dioctanoyl-sn-glycerol (DiC8) neither induced shape change nor a decline in BCECF fluorescence; in contrast BCECF fluorescence rapidly increased indicating an immediate cytosolic alkalinization. Concurrent analysis of [Ca2+]i under conditions in which shape change did not interfere with BCECF fluorescence showed that cytosolic alkalinization and Ca2+ mobilization started almost simultaneously. These observations suggest that cytosolic alkalinization is not preceded by a fall in pHi and can support Ca2+ mobilization induced by weak agonists.
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Jaconi, M. E., D. P. Lew, J. L. Carpentier, K. E. Magnusson, M. Sjögren, and O. Stendahl. "Cytosolic free calcium elevation mediates the phagosome-lysosome fusion during phagocytosis in human neutrophils." Journal of Cell Biology 110, no. 5 (May 1, 1990): 1555–64. http://dx.doi.org/10.1083/jcb.110.5.1555.
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Cytosolic free calcium ([Ca2+]i) and fusion of secondary granules with the phagosomal membrane (phagosome-lysosome fusion, P-L fusion) were assessed in single adherent human neutrophils during phagocytosis of C3bi-opsonized yeast particles. Neutrophils were loaded with the fluorescent dye fura2/AM and [Ca2+]i was assessed by dual excitation microfluorimetry. Discharge of lactoferrin, a secondary granule marker into the phagosome was verified by immunostaining using standard epifluorescence, confocal laser scanning and electron microscopy. In Ca2(+)-containing medium, upon contact with a yeast particle, a rapid rise in [Ca2+]i was observed, followed by one or more Ca2+ peaks (maximal value 1,586 nM and median duration 145 s): P-L fusion was detected in 80% of the cells after 5-10 min. In Ca2(+)-free medium the amplitude, frequency and duration of the [Ca2+]i transients were decreased (maximal value 368 nM, mostly one single Ca2+ peak and median duration 75 s): P-L fusion was decreased to 52%. Increasing the cytosolic Ca2+ buffering capacity by loading the cells with MAPT/AM led to a dose-dependent inhibition both of [Ca2+]i elevations and P-L fusion. Under conditions where basal [Ca2+]i was reduced to less than 20 nM and intracellular Ca2+ stores were depleted, P-L fusion was drastically inhibited while the cells ingested yeast particles normally. P-L fusion could be restored in Ca2(+)-buffered cells containing ingested particles by elevating [Ca2+]i with the Ca2(+)-ionophore ionomycin. The present findings directly indicate that although the ingestion step of phagocytosis is a Ca2(+)-independent event, [Ca2+]i transients triggered upon contact with opsonized particles are necessary to control the subsequent fusion of secondary granules with the phagosomal membrane.
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Bonvini, Sara J., Mark A. Birrell, Eric Dubuis, John J. Adcock, Michael A. Wortley, Pauline Flajolet, Peter Bradding, and Maria G. Belvisi. "Novel airway smooth muscle–mast cell interactions and a role for the TRPV4-ATP axis in non-atopic asthma." European Respiratory Journal 56, no. 1 (April 16, 2020): 1901458. http://dx.doi.org/10.1183/13993003.01458-2019.
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Mast cell–airway smooth muscle (ASM) interactions play a major role in the immunoglobulin (Ig)E- dependent bronchoconstriction seen in asthma but less is known about IgE-independent mechanisms of mast cell activation. Transient receptor potential cation channel, subfamily V, member 4 (TRPV4) activation causes contraction of human ASM via the release of cysteinyl leukotrienes (cysLTs) but the mechanism is unknown. The objective of the present study was to investigate a role for IgE-independent, mast cell–ASM interaction in TRPV4-induced bronchospasm.Bronchoconstriction was measured in anaesthetised guinea pigs and contraction of human and guinea-pig airway tissue assessed using isometric tension measurements. Increases in intracellular [Ca2+] were imaged using the Ca2+-sensitive dye FURA2, and time-lapse ptychography was utilised as a surrogate for contraction of ASM cells.The TRPV4 agonist GSK1016790A caused contraction in vivo in the guinea pig, and in human and guinea-pig tracheal tissue, which was inhibited by the TRPV4 antagonist GSK2193874. GSK1016790A increased [Ca2+]i and released ATP in human ASM cells without causing contraction. TRPV4 and ATP evoked contraction in isolated tracheal tissue but co-culture experiments indicated a requirement for human lung mast cells. Expression profiling and pharmacological studies demonstrated that mast cell activation was dependent upon ATP activating the P2X4 receptor. Trypsin was shown to evoke contraction of tracheal tissue via activation of PAR-2-TRPV4-ATP-cysLT axis indicating the potential disease relevance of this signalling pathway.TRPV4 activation increases [Ca2+]i and releases ATP from ASM cells triggering P2X4-dependent release of cysLTs from mast cells resulting in ASM contraction. This study delineates a novel mast cell–ASM interaction and TRPV4 as a driver of IgE-independent mast cell-dependent bronchospasm.
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Berven, L. A., B. P. Hughes, and G. J. Barritt. "A slowly ADP-ribosylated pertussis-toxin-sensitive GTP-binding regulatory protein is required for vasopressin-stimulated Ca2+ inflow in hepatocytes." Biochemical Journal 299, no. 2 (April 15, 1994): 399–407. http://dx.doi.org/10.1042/bj2990399.
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The roles of heterotrimeric GTP-binding regulatory proteins (G-proteins) and inositol polyphosphates in the mechanism by which vasopressin stimulates Ca2+ inflow in hepatocytes were investigated by using single cells loaded with fura2 by microinjection. Vasopressin-stimulated Ca2+ inflow was mimicked by microinjection of guanosine 5′-[gamma-thio]triphosphate (GTP[S]) or guanosine 5′-[beta gamma-imido]triphosphate to the cells, but not adenosine 5′-[gamma-thio]triphosphate (ATP[S]) or guanosine 5′-[beta-thio]diphosphate (GDP[S]). Extracellular Gd3+ (5 microM) inhibited both vasopressin- and GTP[S]-stimulated Ca2+ inflow. GDP[S], but not GMP, administered to hepatocytes by microinjection, completely inhibited vasopressin-stimulated Ca2+ inflow and partially inhibited vasopressin-induced release of Ca2+ from intracellular stores. The microinjection of pertussis toxin had no effect either on the release of Ca2+ from intracellular stores or on Ca2+ inflow induced by vasopressin, but completely inhibited changes in these processes induced by epidermal growth factor (EGF). Hepatocytes isolated from rats treated with pertussis toxin for 24 h exhibited no vasopressin- or GTP[S]-stimulated Ca2+ inflow, whereas the vasopressin-stimulated release of Ca2+ from intracellular stores was similar to that observed for control cells. Heparin or ATP[S] inhibited, or delayed the onset of, both vasopressin-induced release of Ca2+ from intracellular stores and vasopressin-stimulated Ca2+ inflow. Vasopressin-induced oscillations in intracellular [Ca2+] were observed in some heparin-treated cells. It is concluded that the stimulation by vasopressin of Ca2+ inflow to hepatocytes requires inositol 1,4,5-trisphosphate (InsP3) and, by implication, the pertussis-toxin-insensitive G-protein required for the activation of phospholipase C beta [Taylor, Chae, Rhee and Exton (1991) Nature (London) 350, 516-518], and another G-protein which is slowly ADP-ribosylated by pertussis toxin and acts between InsP3 and the putative plasma-membrane Ca2+ channel. EGF-stimulated Ca2+ inflow involves at least one G-protein which is rapidly ADP-ribosylated and is most likely required for InsP3 formation.
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Robin, Gaëlle, Christine Berthier, and Bruno Allard. "Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control." Journal of General Physiology 139, no. 3 (February 27, 2012): 209–18. http://dx.doi.org/10.1085/jgp.201110738.
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Under resting conditions, external Ca2+ is known to enter skeletal muscle cells, whereas Ca2+ stored in the sarcoplasmic reticulum (SR) leaks into the cytosol. The nature of the pathways involved in the sarcolemmal Ca2+ entry and in the SR Ca2+ leak is still a matter of debate, but several lines of evidence suggest that these Ca2+ fluxes are up-regulated in Duchenne muscular dystrophy. We investigated here SR calcium permeation at resting potential and in response to depolarization in voltage-controlled skeletal muscle fibers from control and mdx mice, the mouse model of Duchenne muscular dystrophy. Using the cytosolic Ca2+ dye Fura2, we first demonstrated that the rate of Ca2+ increase in response to cyclopiazonic acid (CPA)–induced inhibition of SR Ca2+-ATPases at resting potential was significantly higher in mdx fibers, which suggests an elevated SR Ca2+ leak. However, removal of external Ca2+ reduced the rate of CPA-induced Ca2+ increase in mdx and increased it in control fibers, which indicates an up-regulation of sarcolemmal Ca2+ influx in mdx fibers. Fibers were then loaded with the low-affinity Ca2+ dye Fluo5N-AM to measure intraluminal SR Ca2+ changes. Trains of action potentials, chloro-m-cresol, and depolarization pulses evoked transient Fluo5N fluorescence decreases, and recovery of voltage-induced Fluo5N fluorescence changes were inhibited by CPA, demonstrating that Fluo5N actually reports intraluminal SR Ca2+ changes. Voltage dependence and magnitude of depolarization-induced SR Ca2+ depletion were found to be unchanged in mdx fibers, but the rate of the recovery phase that followed depletion was found to be faster, indicating a higher SR Ca2+ reuptake activity in mdx fibers. Overall, CPA-induced SR Ca2+ leak at −80 mV was found to be significantly higher in mdx fibers and was potentiated by removal of external Ca2+ in control fibers. The elevated passive SR Ca2+ leak may contribute to alteration of Ca2+ homeostasis in mdx muscle.
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Zheng, Xian‐Fu, Ying‐Xia Zhou, Hong‐Yun Zhang, Yun‐Yin Niu, Xiao‐Qing Shen, Cao‐Yuan Niu, and Ben‐Lai Wu. "Synthesis, Crystal Structure and Properties of a Novel Cu(II)Complex with α‐Furan Carboxylate, [Cu(fura)2(bpy)(H2O)], (fura=α‐Furan Carboxylate, bpy=2,2′‐bispyridine)." Synthesis and Reactivity in Inorganic, Metal-Organic, and Nano-Metal Chemistry 37, no. 4 (May 1, 2007): 235–39. http://dx.doi.org/10.1080/15533170701316437.
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Zheng, Xian‐Fu, Ying‐Xia Zhou, Hong‐Yun Zhang, Xiao‐Qing Shen, Yun‐Yin Niu, Cao‐Yuan Niu, and Ben‐Lai Wu. "Synthesis, Crystal Structure and Properties of a Novel Cu(II) Complex with α‐Furan Carboxylate, [Cu(fura)2(bpy)(H2O)], (fura=α‐Furan Carboxylate, bpy=2,2′‐bispyridine)." Synthesis and Reactivity in Inorganic, Metal-Organic, and Nano-Metal Chemistry 37, no. 7 (September 1, 2007): 541–45. http://dx.doi.org/10.1080/15533170701563749.
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Baurand, Anthony, Anita Eckly, Nadège Bari, Catherine Léon, Béatrice Hechler, Jean-Pierre Cazenave, and Christian Gachet. "Desensitization of the Platelet Aggregation Response to ADP: Differential Down-regulation of the P2Y1 and P2cyc Receptors." Thrombosis and Haemostasis 84, no. 09 (2000): 484–91. http://dx.doi.org/10.1055/s-0037-1614049.
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SummaryPlatelets activated by ADP become refractory to restimulation, but the mechanism of this process is not well understood. A normal platelet response to ADP requires coactivation of the P2Y1 receptor responsible for shape change and the P2cyc receptor, responsible for completion and amplification of the response. The aim of the present study was to characterize the desensitization of platelets to ADP and to determine whether or not these two receptors are desensitized simultaneously through identical pathways when platelets become refractory to ADP. It was found that full inhibition of platelet aggregation in response to restimulation by ADP required the presence of ADP in the medium or use of a high concentration (1 mM) of its non-hydrolysable analogue ADP β S. Platelets incubated for 1 h at 37° C with 1 mM ADP β S and resuspended in Tyrode’s buffer containing apyrase displayed a stable refractory state characterized by the inability to aggregate or change shape in response to ADP. ADP β S treated platelets loaded with fura2/AM showed complete blockade of the calcium signal in response to ADP, whereas the capacity of ADP to inhibit PGE1 stimulated cAMP accumulation in these platelets was only diminished. Consequently, serotonin was able to promote ADP induced aggregation through activation of the Gq coupled 5HT2A receptor while adrenaline had no such effect. These results suggested that the refractory state of ADP β S treated platelets was entirely due to desensitization of the P2Y1 receptor, the P2cyc receptor remaining functional. Binding studies were performed to determine whether the P2Y1 and/or P2cyc binding sites were modified in refractory platelets. Using selective P2Y1 and P2cyc antagonists (A3P5P and AR-C66096 respectively), we could demonstrate that the decrease in [33P]2MeSADP binding sites on refractory platelets corresponded to disappearance of the P2Y1 sites with no change in the number of P2cyc sites, suggesting internalization of the P2Y1 receptor. This was confirmed by flow cytometric analysis of Jurkat cells expressing an epitope-tagged P2Y1 receptor, where ADP β S treatment resulted in complete loss of the receptor from the cell surface. We conclude that the P2Y1 and P2cyc receptors are differently regulated during platelet activation.
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Vranová, J., and Z. Ciesarová. "Furan in food – a review." Czech Journal of Food Sciences 27, No. 1 (February 11, 2009): 1–10. http://dx.doi.org/10.17221/2843-cjfs.
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Furan and its derivatives were identified in a small number of heat-treated foods back in the 60’s and 70’s. In May 2004, US Food and Drug Administration published a report on the occurrence of parent furan in a number of thermally treated foods. Since furan has been classified as “possibly carcinogenic to human” by IARC, a great concern has been addressed to the analysis of this substance naturally-occurring in food. This paper gives a short overview on the mechanistic pathways of the parent furan formation in food by degradation of amino acids and/or reducing sugars, and oxidation of ascorbic acid and poly-unsaturated acids which can be induced by thermal or irradiation treatments; further, it deals with the metabolism and toxicology of furan as well as with the comparison of the methods of furan determination.
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Gao, Junyuan, Xiurong Sun, Francisco J. Martinez-Wittinghan, Xiaohua Gong, Thomas W. White, and Richard T. Mathias. "Connections Between Connexins, Calcium, and Cataracts in the Lens." Journal of General Physiology 124, no. 4 (September 27, 2004): 289–300. http://dx.doi.org/10.1085/jgp.200409121.
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There is a good deal of evidence that the lens generates an internal micro circulatory system, which brings metabolites, like glucose, and antioxidants, like ascorbate, into the lens along the extracellular spaces between cells. Calcium also ought to be carried into the lens by this system. If so, the only path for Ca2+ to get out of the lens is to move down its electrochemical gradient into fiber cells, and then move by electrodiffusion from cell to cell through gap junctions to surface cells, where Ca-ATPase activity and Na/Ca exchange can transport it back into the aqueous or vitreous humors. The purpose of the present study was to test this calcium circulation hypothesis by studying calcium homeostasis in connexin (Cx46) knockout and (Cx46 for Cx50) knockin mouse lenses, which have different degrees of gap junction coupling. To measure intracellular calcium, FURA2 was injected into fiber cells, and the gradient in calcium concentration from center to surface was mapped in each type of lens. In wild-type lenses the coupling conductance of the mature fibers was ∼0.5 S/cm2 of cell to cell contact, and the best fit to the calcium concentration data varied from 700 nM in the center to 300 nM at the surface. In the knockin lenses, the coupling conductance was ∼1.0 S/cm2 and calcium varied from ∼500 nM at the center to 300 nM at the surface. Thus, when the coupling conductance doubled, the concentration gradient halved, as predicted by the model. In knockout lenses, the coupling conductance was zero, hence the efflux path was knocked out and calcium accumulated to ∼2 μM in central fibers. Knockout lenses also had a dense central cataract that extended from the center to about half the radius. Others have previously shown that this cataract involves activation of a calcium-dependent protease, Lp82. We can now expand on this finding to provide a hypothesis on each step that leads to cataract formation: knockout of Cx46 causes loss of coupling of mature fiber cells; the efflux path for calcium is therefore blocked; calcium accumulates in the central cells; at concentrations above ∼1 μM (from the center to about half way out of a 3-wk-old lens) Lp82 is activated; Lp82 cleaves cytoplasmic proteins (crystallins) in central cells; and the cleaved proteins aggregate and scatter light.
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Rafael Lopez, Jose, Vikas Kaura, Phillip Hopkins, Xiaochen Liu, Arkady Uryach, Jose Adams, and Paul D. Allen. "Transient Receptor Potential Cation Channels and Calcium Dyshomeostasis in a Mouse Model Relevant to Malignant Hyperthermia." Anesthesiology 133, no. 2 (June 5, 2020): 364–76. http://dx.doi.org/10.1097/aln.0000000000003387.
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Background Until recently, the mechanism for the malignant hyperthermia crisis has been attributed solely to sustained massive Ca2+ release from the sarcoplasmic reticulum on exposure to triggering agents. This study tested the hypothesis that transient receptor potential cation (TRPC) channels are important contributors to the Ca2+ dyshomeostasis in a mouse model relevant to malignant hyperthermia. Methods This study examined the mechanisms responsible for Ca2+ dyshomeostasis in RYR1-p.G2435R mouse muscles and muscle cells using calcium and sodium ion selective microelectrodes, manganese quench of Fura2 fluorescence, and Western blots. Results RYR1-p.G2435R mouse muscle cells have chronically elevated intracellular resting calcium and sodium and rate of manganese quench (homozygous greater than heterozygous) compared with wild-type muscles. After exposure to 1-oleoyl-2-acetyl-sn-glycerol, a TRPC3/6 activator, increases in intracellular resting calcium/sodium were significantly greater in RYR1-p.G2435R muscles (from 153 ± 11 nM/10 ± 0.5 mM to 304 ± 45 nM/14.2 ± 0.7 mM in heterozygotes P < 0.001] and from 251 ± 25 nM/13.9 ± 0.5 mM to 534 ± 64 nM/20.9 ± 1.5 mM in homozygotes [P < 0.001] compared with 123 ± 3 nM/8 ± 0.1 mM to 196 ± 27 nM/9.4 ± 0.7 mM in wild type). These increases were inhibited both by simply removing extracellular Ca2+ and by exposure to either a nonspecific (gadolinium) or a newly available, more specific pharmacologic agent (SAR7334) to block TRPC6- and TRPC3-mediated cation influx into cells. Furthermore, local pretreatment with SAR7334 partially decreased the elevation of intracellular resting calcium that is seen in RYR1-p.G2435R muscles during exposure to halothane. Western blot analysis showed that expression of TRPC3 and TRPC6 were significantly increased in RYR1-p.G2435R muscles in a gene–dose–dependent manner, supporting their being a primary molecular basis for increased sarcolemmal cation influx. Conclusions Muscle cells in knock-in mice expressing the RYR1-p.G2435R mutation are hypersensitive to TRPC3/6 activators. This hypersensitivity can be negated with pharmacologic agents that block TRPC3/6 activity. This reinforces the working hypothesis that transient receptor potential cation channels play a critical role in causing intracellular calcium and sodium overload in malignant hyperthermia–susceptible muscle, both at rest and during the malignant hyperthermia crisis. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New
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De Santis, T., M. E. Dell'Aquila, F. Maritato, V. Casavola, and P. Minoia. "280 EFFECTS OF β-ENDORPHIN AND NALOXONE ON INTRACELLULAR CALCIUM LEVELS IN CUMULUS CELLS OF EQUINE OOCYTES." Reproduction, Fertility and Development 17, no. 2 (2005): 290. http://dx.doi.org/10.1071/rdv17n2ab280.
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Changes in intracellular calcium levels in the cumulus oocyte complex (COC) have a crucial role in oocyte maturation. In previous studies we demonstrated that the μ-opioid receptor is expressed in the bovine COC and participates in the signaling associated with oocyte maturation, by inducing an intracellular calcium increase (Dell'Aquila ME et al. 2002 Mol. Reprod. Dev. 63, 210–222). In this work we evaluated modifications of intracellular calcium induced by β-endorphin (β-end) or Naloxone (Nx) in cumulus cells of equine oocytes in relation to the time of the year and cumulus morphology at retrieval. Cumulus cells, isolated by mechanical treatment from compact (Cp, n = 120) or expanded (Exp, n = 120) COCs, recovered from the ovaries of slaughtered mares (follicles <20 mm in diameter) during anestrus, breeding season, spring transition, and autumnal transition, were cultured for 24 h and loaded with 5 μM Fura2-AM for microspectrofluorometric measurements of cytoplasmic ionized calcium (Dell'Aquila et al., 2002). The changes in β-end (30 μM)- or Nx (1mM and 10 μM)-induced calcium concentration were calculated in single cells (n = 194) and are expressed as Δ fluorescence (Fmaximal effect – Fbaseline) before and after 1-min perfusion with the drugs. The use of 1 mM Nx induced a significant increase of intracellular calcium levels in cumulus cells of oocytes recovered in all periods of the year in both Cp and Exp (P < 0.01). The addition of 10 μM Nx or 30 μM β-end significantly increased intracellular calcium only in cumulus cells from oocytes recovered in anestrus (P < 0.05). These results confirm previous observations, carried out on bovine oocytes, in which Nx behaved as a μ-receptor agonist when used at high concentration (Dell'Aquila et al. 2002). The effects of β-end and Nx may be explained in terms of a binding of the two subtances at the μ-receptor with consequent intracellular calcium increases due to extracellular calcium entry or depletion of intracellular stores. These findings could be related to differential espression and/or activation status of the μ-opioid receptor in COCs retrieved in different seasons. These substances can be used to modulate intracellular calcium in the equine COCs, and consequent effects on the stimulation/inhibition of oocyte maturation in this species need to be further investigated. This work was supported by Grant MIUR COFIN PRIN 2003.
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Lorenzon, P., E. Vecile, E. Nardon, E. Ferrero, J. M. Harlan, F. Tedesco, and A. Dobrina. "Endothelial Cell E- and P-Selectin and Vascular Cell Adhesion Molecule-1 Function as Signaling Receptors." Journal of Cell Biology 142, no. 5 (September 7, 1998): 1381–91. http://dx.doi.org/10.1083/jcb.142.5.1381.
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Previous studies have shown that polymorphonuclear leukocyte (PMN) adherence to endothelial cells (EC) induces transient increases in EC cytosolic free calcium concentration ([Ca2+]i) that are required for PMN transit across the EC barrier (Huang, A.J., J.E. Manning, T.M. Bandak, M.C. Ratau, K.R. Hanser, and S.C. Silverstein. 1993. J. Cell Biol. 120:1371–1380). To determine whether stimulation of [Ca2+]i changes in EC by leukocytes was induced by the same molecules that mediate leukocyte adherence to EC, [Ca2+]i was measured in Fura2-loaded human EC monolayers. Expression of adhesion molecules by EC was induced by a pretreatment of the cells with histamine or with Escherichia coli lipopolysaccharide (LPS), and [Ca2+]i was measured in single EC after the addition of mAbs directed against the EC adhesion proteins P-selectin, E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), or platelet/endothelial cell adhesion molecule-1 (PECAM-1). Both anti–P- and anti–E-selectin mAb, as well as anti–VCAM-1 mAb, induced transient increases in EC [Ca2+]i that were comparable to those induced by 200 μM histamine. In contrast, no effect was obtained by mAbs directed against the endothelial ICAM-1 or PECAM-1. PMN adherence directly stimulated increases in [Ca2+]i in histamine- or LPS-treated EC. mAbs directed against leukocyte CD18 or PECAM-1, the leukocyte counter-receptors for endothelial ICAM-1 and PECAM-1, respectively, did not inhibit PMN-induced EC activation. In contrast, mAb directed against sialyl Lewis x (sLex), a PMN ligand for endothelial P- and E-selectin, completely inhibited EC stimulation by adherent PMN. Changes in EC [Ca2+]i were also observed after adherence of peripheral blood monocytes to EC treated with LPS for 5 or 24 h. In these experiments, the combined addition of mAbs to sLex and VLA-4, the leukocyte counter-receptor for endothelial VCAM-1, inhibited [Ca2+]i changes in the 5 h–treated EC, whereas the anti–VLA-4 mAb alone was sufficient to inhibit [Ca2+]i changes in the 24 h-treated EC. Again, no inhibitory effect was observed with an anti-CD18 or anti–PECAM-1 mAb. Of note, the conditions that induced changes in EC [Ca2+]i, i.e., mAbs directed against endothelial selectins or VCAM-1, and PMN or monocyte adhesion to EC via selectins or VCAM-1, but not via ICAM-1 or PECAM-1, also induced a rearrangement of EC cytoskeletal microfilaments from a circumferential ring to stress fibers. We conclude that, in addition to their role as adhesion receptors, endothelial selectins and VCAM-1 mediate endothelial stimulation by adhering leukocytes.
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Kulkarni, G. V., and C. A. McCulloch. "Serum deprivation induces apoptotic cell death in a subset of Balb/c 3T3 fibroblasts." Journal of Cell Science 107, no. 5 (May 1, 1994): 1169–79. http://dx.doi.org/10.1242/jcs.107.5.1169.
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Little is known about the regulation of apoptosis in fibroblasts although several model systems including serum deprivation and treatment with staurosporine or topoisomerase inhibitors have been used to induce apoptosis in vitro. To validate a reproducible in vitro model for the study of apoptosis in fibroblasts, we cultured density-inhibited monolayer cultures of Balb/c 3T3 fibroblasts in Dulbecco's modified essential medium plus 15% fetal calf serum and then withdrew serum. Time-lapse video microscopy demonstrated that within minutes of serum withdrawal, cells lost substrate attachment and floated to the top of the liquid growth medium. There was a time-dependent increase in the number of non-adherent cells. Some of these cells regained attachment and spread momentarily, but they eventually rounded up and lost attachment permanently. In contrast to serum-containing cultures in which similar morphological changes were followed by mitosis, in serum-free cultures repeated attempts at mitosis were followed by permanent attachment loss and presumably cell death. To assess whether all the non-adherent cells were in fact dead, the percentages of cells that continued to proliferate upon return to serum-supplemented conditions was computed. After various periods of serum starvation a decreasing proportion (approx. 75% at 30 minutes; < 2% at 24 hours) of the non-adherent cells could be rescued by addition of serum. Transmission electron microscopy of cells 3 hours after serum withdrawal showed that the majority (approximately 60%) of non-adherent cells exhibited marked intranuclear chromatin condensation but maintained integrity of cell and nuclear membranes and cell organelles, morphological changes consistent with those of apoptotic cell death. Scanning electron microscopy of cultures 3 hours following serum withdrawal showed rounded cells with marked surface blebbing. Fluorescence and confocal microscopy revealed increased intensity of nuclear staining with DAPI while actin filaments became indistinct or collapsed around the nucleus. After cycloheximide treatment to inhibit protein synthesis, there was no reduction of apoptosis. Gel electrophoresis of DNA from both control and 3 hour-serum-deprived cells showed intact DNA with no oligonucleosomal length fragmentation. After serum withdrawal, intracellular calcium was reduced by about 32% over 5 minutes as measured by fura2 ratio fluorimetry in single cells. Serum-starved cells showed a time-dependent shrinkage in mean cell diameter compared to trypsinized, adherent control cells (at 0 hours, mean diameter = 18.0 microns--viable; at 4 hours, mean diameter = 15.5 microns--apoptotic). Flow cytometric analysis showed increased propidium iodide staining and reduced fluorescein diacetate uptake over 3 hours, changes that were contemporaneous with the reduction of cell diameter.(ABSTRACT TRUNCATED AT 400 WORDS)
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Kaya, Emre, Seval Yılmaz, and Songul Ceribasi. "Protective role of propolis on low and high dose furan-induced hepatotoxicity and oxidative stress in rats." Journal of Veterinary Research 63, no. 3 (September 13, 2019): 423–31. http://dx.doi.org/10.2478/jvetres-2019-0054.
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Abstract Introduction The aim of this study was to evaluate potential protective effects of propolis on furan-induced hepatic damage by assessing the levels of malondialdehyde (MDA) and reduced glutathione (GSH), antioxidant enzyme activities, and histopathological changes in the liver. Material and Methods Albino Wistar rats were divided into six groups: a control, propolis-treated (100 mg/kg b.w./day), low-dose furan-treated (furan-L group; 2 mg/kg b.w./day), high-dose furan-treated (furan-H group; 16 mg/kg b.w./day), furan-L+propolis treated, and furan-H+propolis treated group. Propolis and furan were applied by gavage; propolis for 8 days, and furan for 20 days in furan-L groups and 10 days in furan-H groups. ResultsWhile MDA levels were elevated in furan-treated groups, levels of GSH and activities of antioxidant enzymes decreased (p < 0.001). The levels of MDA and GSH and activities of antioxidant enzymes were normal in the furan+propolis groups, especially in the furan-L+propolis group (p < 0.001). While the aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate pdehydrogenase activities were elevated in the furan-H treated group (p < 0.05 and p < 0.001), they were unchanged in the furan-L treated group. Histopathologically, several lesions were observed in the liver tissues of the furan-treated groups, especially in the higher-dose group. It was determined that these changes were milder in both of the furan+propolis groups. Conclusion The results indicate that propolis exhibits good hepatoprotective and antioxidant potential against furan-induced hepatocellular damage in rats.
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Janczewski, Łukasz, Dariusz Zieliński, and Beata Kolesińska. "Synthesis of amides and esters containing furan rings under microwave-assisted conditions." Open Chemistry 19, no. 1 (January 1, 2021): 265–80. http://dx.doi.org/10.1515/chem-2021-0034.
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Abstract In this work, we present a novel method for the synthesis of ester and amide derivatives containing furan rings (furfural derivatives) under mild synthetic conditions supported by microwave radiation. N-(Furan-2-ylmethyl)furan-2-carboxamide and furan-2-ylmethyl furan-2-carboxylate were produced using 2-furoic acid, furfurylamine, and furfuryl alcohol. The reactions were carried out in a microwave reactor in the presence of effective coupling reagents: DMT/NMM/TsO− or EDC. The reaction time, the solvent, and the amounts of the substrates were optimized. After crystallization or flash chromatography, the final compounds were isolated with good or very good yields. Our method allows for the synthesis of N-blocked amides using N-blocked amino acids (Boc, Cbz, Fmoc) and amine. As well as compounds with a monoamide and ester moiety, products with diamides and diester bonds (N,N-bis(furan-2-ylmethyl)furan-2,5-dicarboxamide, bis(furan-2-ylmethyl) furan-2,5-dicarboxylate, and furan-3,4-diylbis(methylene) bis(furan-2-carboxylate)) were synthesized with moderate yields in the presence of DMT/NMM/TsO– or EDC, using 2,5-furandicarboxylic acid and 3,4-bis(hydroxymethyl)furan as substrates.
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Albrand, Michel, René Dolmazon, and Patrick Pollet. "Synthèse, structure et études spectroscopiques RMN 1H et 13C de dérivés perhydrocyclododéca[b]furaniques." Canadian Journal of Chemistry 69, no. 3 (March 1, 1991): 521–27. http://dx.doi.org/10.1139/v91-078.
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A synthetic route to perhydrocyclododeca[b]furan-3-ols, perhydrocyclododeca[b]furan-3-ones, and perhydrocyclododeca[b]furan derivatives is described. Their configurations were determined. For the perhydrocyclododeca[b]furan-3-one and perhydrocyclododeca[b]furan pairs, the cis isomer was much less stable than the trans isomer. This agrees well with results from a conformational analysis, carried out by molecular mechanics. The 1H and l3C NMR spectra are reported. Key words: perhydrocyclododeca[b]furans, conformations, force field calculations, 1H and 13C NMR.
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Buttery, JH, J. Moursounidis, and D. Wege. "A,B-Diheteropentalenes by a Tandem Intramolecular Diels-Alder/Reverse Diels-Alder Reaction Sequence. Application to the Synthesis of Thieno[3,4-b]furan." Australian Journal of Chemistry 48, no. 3 (1995): 593. http://dx.doi.org/10.1071/ch9950593.
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Alkylation of 2-furylmethanethiol (28) with propargyl chloride gave the thioether (22) which on methoxycarbonylation afforded the acetylenic ester (30). On heating, this material underwent an intramolecular Diels -Alder reaction to give the tricyclic compound (32). In the presence of 3,6- di (pyridin-2′-yl)-s- tetrazine , (32) afforded methyl 4,6-dihydrothieno[3,4-b]furan-3-carboxylate (38) by a sequence involving a further Diels -Alder reaction followed by two reverse Diels-Alder reactions. The ester (38) could be dehydrogenated to give methyl thieno [3,4-b]furan-3-carboxylate (40) while hydrolysis of (38), followed by decarboxylation and dehydrogenation delivered the parent thieno [3,4-b]furan (5). 3-Methyl-4,6-dihydrothieno[3,4-b]furan (46) and 3-methylthieno[3,4-b]furan (47) were prepared; a comparison of the 4JMe-C=C-H coupling constants in the 1H n.m.r . spectra of (46) and (47) suggests that an increase in the C2-C3 furyl bond order accompanies the (46) → (47) conversion. Methyl 4,6-dihydrofuro[3,4-b]furan-3-carboxylate (39), 4,6-dihydrofuro[3,4-b]furan (27) and methyl 4,6-dihydro-6-phenylfuro[3,4-b]furan-3-carboxylate (53) were prepared by an analogous tandem reaction sequence. These compounds could not be dehydrogenated to the fully conjugated furo [3,4-b]furan ring system.
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Fromberg, A., M. S. Mariotti, F. Pedreschi, S. Fagt, and K. Granby. "Furan and alkylated furans in heat processed food, including home cooked products ." Czech Journal of Food Sciences 32, No. 5 (October 1, 2014): 443–48. http://dx.doi.org/10.17221/341/2013-cjfs.
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The occurrence of furan in home cooked food was studied. Cooking was found to reduce the level of furan in ready-to-eat foods, however on average around 50% of furan remain in the foods. The analysis of furan occurrence revealed that it is most commonly formed in foods with high levels of carbohydrates. Interestingly, breakfast cereals, dry bread products, and dried fruit products including raisins, plums and bananas contained furan at levels up to 387 µg/kg. Furan was also found in the dry ingredients of cookies and bread, and in snacks such as crisps and popcorn. The 2-alkylfurans, 2-methylfuran, 2,5-dimethylfuran, 2-ethylfuran, and 2-pentylfuran were present at levels in the same range as furan (885 µg/kg) and the level of 2-methylfuran (1328 µg/kg) exceeded this level in coffee.
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Baş, Hatice, Dilek Pandır, and Suna Kalender. "Furan-induced hepatotoxic and hematologic changes in diabetic rats: the protective role of lycopene." Archives of Industrial Hygiene and Toxicology 67, no. 3 (September 1, 2016): 194–203. http://dx.doi.org/10.1515/aiht-2016-67-2762.
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Abstract Furan forms as a result of thermal treatment of food and induces harmful effects on organisms. In our work, lycopene, furan, and a combination of the two were given to diabetic male rats for 28 days. Hematological changes, total protein and cholesterol, triglyceride, and albumin levels, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase activities of the serum, malondialdehyde levels, glutathione peroxidase, catalase, glutathione-S-transferase, superoxide dismutase activities, DNA damage in liver tissues and hepatic histopathological alterations were compared to a control group. There were significant changes in the liver function tests, DNA damage, activities of antioxidant enzymes, and malondialdehyde levels between diabetic control and non-diabetic control groups, between diabetic control and diabetic lycopene groups, and also between diabetic furan and diabetic control groups. In diabetic lycopene and diabetic furan + lycopene treated groups we designated the preventive effects of lycopene against diabetes and furan, however, on the analysed parameters only. In spite of some pathological alterations designated in diabetic furan treated group’s liver, fewer pathological alterations were observed in furan+lycopene treated groups at the end of week 4. Consequently, lycopene significantly reduced furan- and diabetes-induced toxicity in rat liver.
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Takasu, Shinji, Yuji Ishii, Aki Kijima, Kumiko Ogawa, Sae Nakane, and Takashi Umemura. "Furan Induced Characteristic Glutathione S-Transferase Placental Form-Positive Foci in Terms of Cell Kinetics and Gene Expression." Toxicologic Pathology 48, no. 6 (August 2020): 756–65. http://dx.doi.org/10.1177/0192623320948782.
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Glutathione S-transferase placental form-positive (GST-P+) foci are markers of preneoplastic lesions in rat hepatocarcinogenesis. Our previous studies using reporter gene transgenic rats showed that furan, a hepatocarcinogen in rodents, rapidly induces the formation of GST-P+ foci after short exposure without reporter gene mutation. We hypothesized that GST-P+ foci induced by furan may have biological characteristics different from those induced by diethylnitrosamine (DEN), a genotoxic hepatocarcinogen. Accordingly, we compared the cell kinetics of GST-P+ foci after cessation of DEN treatment and performed comprehensive gene expression in DEN- or furan-induced GST-P+ foci. The number and area of DEN-induced GST-P+ foci were increased after cessation of treatment, whereas furan decreased these parameters. Size distribution analysis showed that large furan-induced GST-P+ foci disappeared after cessation of treatment. Hierarchical cluster analysis showed that all samples from GST-P+ foci induced by furan were separated from those induced by DEN. SOX9 expression was upregulated in furan-induced GST-P+ foci and was detected by immunohistochemistry in large furan-induced GST-P+ foci. Our results indicated that large furan-induced GST-P+ foci were quite different from DEN-induced GST-P+ foci at the molecular and cellular levels. And one of the properties of disappearing large GST-P+ foci were characterized by inclusion of hepatocytes expressing SOX9.
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Miret-Casals, Laia, Willem Vannecke, Kurt Hoogewijs, Gianluca Arauz-Garofalo, Marina Gay, Mireia Díaz-Lobo, Marta Vilaseca, Christophe Ampe, Marleen Van Troys, and Annemieke Madder. "Furan warheads for covalent trapping of weak protein–protein interactions: cross-linking of thymosin β4 to actin." Chemical Communications 57, no. 49 (2021): 6054–57. http://dx.doi.org/10.1039/d1cc01731d.
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Furan is used as a caged warhead to covalently target weak protein–protein interactions. Furan-thymosin β4 cross-links selectively and irreversibly with actin targeting lysine. Furan technology could be further exploited for covalent drug design.
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Tǎbǎran, Alexandru-Flaviu, M. Gerard O’Sullivan, Donna E. Seabloom, Karin R. Vevang, William E. Smith, Timothy S. Wiedmann, and Lisa A. Peterson. "Inhaled Furan Selectively Damages Club Cells in Lungs of A/J Mice." Toxicologic Pathology 47, no. 7 (August 19, 2019): 842–50. http://dx.doi.org/10.1177/0192623319869306.
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Furan, a possible human carcinogen, is a product of incomplete combustion and is present in cigarette smoke, engine exhaust, and processed food. Oral administration induces liver toxicity and carcinogenesis in F344 rats and B6C3F1 mice. To assess possible adverse effects from inhalation, A/J mice were nose-only exposed for 3 hours to furan (0, 30, 75, 150, 300, or 600 ppmv) and euthanized after 24 hours, 48 hours, or 1 week. Histopathology evaluation revealed bronchiolar club cell necrosis (diffuse, marked) with airway denudation following exposure to 300 and 600 ppmv furan with evidence of club cell regeneration and partial repair after 1 week. Initial signs of hepatotoxicity were observed in the 150 ppmv furan-exposed group. Acute necrosis and mineralization were observed in livers at 24 and 48 hours with hepatocyte regeneration by 1-week postexposure in mice exposed to 300 and 600 ppmv furan; the 300 ppmv exposed group had multifocal mineralization that evoked a mild granulomatous response. Measurement of urinary furan metabolites confirmed that the mice metabolized furan to the toxic intermediate, cis-2-butene-1,4-dial. These observations indicate that inhaled furan is toxic to lungs with club cells as the target as well as liver.
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Kang, Ha-Na, Da-Mi Jung, and Jung-Hyun Sok. "Synthesis of Double-walled Carbon Nanotubes Using Decomposition of Tetra Hydro Furan." Journal of the Korean Vacuum Society 17, no. 6 (November 30, 2008): 576–81. http://dx.doi.org/10.5757/jkvs.2008.17.6.576.
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Rhee, Seung Whee. "A Study on Thermal Stabilization of Spent Foundry Sand." Materials Science Forum 544-545 (May 2007): 507–10. http://dx.doi.org/10.4028/www.scientific.net/msf.544-545.507.
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Thermal stabilization is used to reduce the turbidity of spent foundry sands (SFSs). Effect of stabilized temperature and thermal stabilized time in thermal stabilization is estimated by turbidity of SFSs in thermal stabilization. The turbidity of furan sand is 984 FAU and almost 15 times as high as that of other sands such as CO2 sand and green sand. Furan sand contains furan resin, but CO2 sand and green sand do not use resin chemicals. The turbidity of furan sand can be reduced by stabilization of furan resin in thermal process. In the process of thermal stabilization, fixation of furan resin by heating occurs and resin can be in the state of insolubility. The turbidity of furan sand is sharply decreased within thermally stabilized time of 2 hrs and decreased with increasing stabilized temperature. Turbidity in thermal stabilized time of 2hrs and stabilized temperature of 600°C is almost 10 FAU. Hence, thermal stabilization can be applied to reduce the turbidity of SFSs generated from iron foundry industry.
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Tucker, Sheryl A., William E. Acree, Maximilian Zander, Pierre Demerseman, and Jean-Pierre Buisson. "Spectroscopic Properties of Polycyclic Aromatic Compounds. Part III: Fluorescence Emission and Quenching Behavior of Periodic Table Group 16 Hetero-Atom Derivatives." Applied Spectroscopy 47, no. 3 (March 1993): 317–20. http://dx.doi.org/10.1366/0003702934066622.
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Fluorescence emission spectra are reported for benzo[b]naphtho[2,3d]furan, dinaphtho[l,2b:l′,2′d]furan, dinaphtho[2,lb:l′,2′d]furan, dibenzo[2,3:10,11]perylo[l,12bcd]furan, dibenzo[2,3:10,ll]perylo-(l,12bcd]thiophene, naphtho[l,8bc:5,4b′c′]dipyran (also called 1,6-dioxapyrene), and naphtha[l,8bc:4,5b′c′]dipyran (also called 1,8-dioxapyrene) in organic nonelectrolyte solvents of varying polarity. Results of these measurements indicate that dinaphtho[l,2b:l′,2′d]furan exhibits slight signs of probe character as evidenced by changing emission intensity ratios; however, the dynamic range was much too small to classify this molecule as a polycyclic aromatic compound probe. The effect of nitromethane and 1,2,4-trimethoxybenzene as selective quenching agents was also examined. Nitromethane was found to quench fluorescence emission of all the aforementioned compounds except benzo[b]naphtho[2,3d]furan.
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Geburtig, Felix, and Volkmar Vill. "2-O-Monoalkyl isosorbide ethers with C8, C10, C12 and C14 chain lengths." Acta Crystallographica Section E Crystallographic Communications 76, no. 6 (May 29, 2020): 924–28. http://dx.doi.org/10.1107/s2056989020006647.
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The title compounds, 6-(octyloxy)hexahydrofuro[3,2-b]furan-3-ol, C14H26O4, 6-(decyloxy)hexahydrofuro[3,2-b]furan-3-ol, C16H30O4, 6-(dodecyloxy)hexahydrofuro[3,2-b]furan-3-ol, C18H34O4, and 6-(tetradecyloxy)hexahydrofuro[3,2-b]furan-3-ol, C20H38O4, consist of a polar headgroup (isosorbide) and a lipophilic alkyl chain linked via an ether bridge. Isosorbide is a biobased diol, containing two fused furan rings. One intermolecular hydrogen bond connects the molecules between the free endo hydroxy group and the opposing ether oxygen of the V-shaped head group. Thus the molecule layers interlock like in a herringbone pattern parallel to the bc plane.
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Becalski, Adam, and Stephen Seaman. "Furan Precursors in Food: A Model Study and Development of a Simple Headspace Method for Determination of Furan." Journal of AOAC INTERNATIONAL 88, no. 1 (January 1, 2005): 102–6. http://dx.doi.org/10.1093/jaoac/88.1.102.
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Abstract Furan was previously detected in foods that had undergone thermal treatment. Because furan is now classified as a possible human carcinogen, a model system was developed to investigate the origins of furan. Also, a simple, rapid isotope dilution (d4-furan) headspace method was developed to measure furan. Two pathways of furan formation have been identified in the model systems tested so far. The first is the oxidation of polyunsaturated fatty acids at elevated temperatures, and the second is linked to the decomposition of ascorbic acid derivatives. The analytical procedure, based on the use of a 50 μL injection (from the headspace of a 1.5 mL vial containing 0.5 mL water) into the split/splitless injection port of a gas chromatograph/mass spectrometer (electron ionization, selected-ion monitoring), showed linearity in the 10–1000 ng/g range with a limit of detection of 1 ng/g.