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Journal articles on the topic 'Inositolphosphates'

Author: Grafiati

Published: 16 February 2023

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1

Etoh, S., M. Ohashi, A. Baba, and H. Iwata. "Ibudilast inhibits inositolphosphates formation in guinea pig lung." European Journal of Pharmacology 183, no. 3 (July 1990): 761–62. http://dx.doi.org/10.1016/0014-2999(90)92565-z.

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2

Kvasnička, František, Jana Čopíková, Rudolf Ševčík, Eliška Václavíková, Andriy Synytsya, Kateřina Vaculová, and Michal Voldřich. "Determination of phytic acid and inositolphosphates in barley." ELECTROPHORESIS 32, no. 9 (March 31, 2011): 1090–93. http://dx.doi.org/10.1002/elps.201000578.

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3

Tian, Yuemin, Rainer Schreiber, Podchanart Wanitchakool, Patthara Kongsuphol, Marisa Sousa, Inna Uliyakina, Marta Palma, et al. "Control of TMEM16A by INO-4995 and other inositolphosphates." British Journal of Pharmacology 168, no. 1 (December 18, 2012): 253–65. http://dx.doi.org/10.1111/j.1476-5381.2012.02193.x.

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4

Whelan, J. P., W. T. Shearer, E. B. Gilliam, and K. J. Hardy. "A protein kinase C-activating phorbol ester accelerates the T cell antigen receptor-stimulated phosphatidylinositol cycle in normal human CD4+ T cells." Journal of Immunology 148, no. 9 (May 1, 1992): 2872–78. http://dx.doi.org/10.4049/jimmunol.148.9.2872.

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Abstract Ligation of the TCR on Jurkat T lymphoblastoid cells causes an 1,4,5-inositol trisphosphate-dependent rise in intracellular cytoplasmic calcium that is inhibited by PMA, a potent activator of protein kinase C. Consequently, protein kinase C is widely believed to mediate feedback inhibition of TCR-activated phospholipase C. We have now extended these studies to normal unblasted human CD4+ T lymphocytes, examining the PMA sensitivity of both the TCR complex-mediated release of total inositol-phosphates and the resynthesis of the parent phosphoinositides. In contrast to Jurkat, in which PMA inhibited release of 1,4,5-inositol trisphosphate by 60% and total inositolphosphates by 40% (50% inhibitory concentration, 5.6 nM), normal cells displayed a marked increase in anti-CD3-induced phosphatidylinositol (PI) cycling in the presence of PMA. Both total inositolphosphate release and PI resynthesis were maximally elevated (88% and 342%, respectively) by a PMA concentration that also optimally supported a subsequent proliferative response; the ED50 was at least 11.7-fold lower than that for the inhibitory effect of PMA on breakdown of total Jurkat PI. A PKC nonactivating phorbol ester had no effect. If anti-CD3 was replaced by the mitogenic lectin PHA, PI resynthesis was similarly up-regulated by PMA in these highly purified cells. The PMA up-regulatory phenomenon was not a simple consequence of cell blastogenesis, inasmuch as there was no early effect on the non-signaling-associated phosphatidylethanolamine compartment after CD3 stimulation. Thus, PKC activation appears to accelerate TCR-linked PI metabolism in normal Th cells, in contrast to the feedback inhibitor paradigm observed in Jurkat and other tumor cell systems.

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5

Treves, S., F. Di Virgilio, V. Cerundolo, P. Zanovello, D. Collavo, and T. Pozzan. "Calcium and inositolphosphates in the activation of T cell-mediated cytotoxicity." Journal of Experimental Medicine 166, no. 1 (July 1, 1987): 33–42. http://dx.doi.org/10.1084/jem.166.1.33.

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Reports from a number of laboratories have shown that mAbs against the T3-Ti receptor complex cause an increase in cytosolic-free Ca2+ [( Ca2+]i) and the hydrolysis of phosphatidylinositolbisphosphate (PIP2) in CTLs. In the present report we show that activation of CTLs by their specific targets causes: (a) release of Ca2+ from intracellular stores; (b) transient formation of inositol trisphosphate (InsP3); and (c) an increased permeability to Ca2+ of CTL plasma membrane. Killing of unrelated targets could be induced by cocentrifugation of the unrelated targets with CTLs in the presence of A23187 or PMA. We conclude that: (a) activation of CTLs by specific antigens triggers the generation of the same intracellular mediators generated by stimulation of lymphocytes with anti-T3-Ti receptor antibodies and/or with polyclonal mitogens; and (b) intracellular signals that mediate the delivery of the lethal hit by CTLs are indistinguishable from those that induce cell proliferation.

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6

Bogdanowicz, P., and JP Pujol. "Rôle des inositolphosphates glycanes dans la signalisation intracellulaire : relations avec la pathologie." médecine/sciences 17, no. 5 (2001): 577. http://dx.doi.org/10.4267/10608/1970.

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7

Sorokina, I. V., I. V. Borzenkova, M. S. Myroshnychenko, O. M. Pliten, O. A. Omelchenko, and A. V. Simachova. "Content of inositolphosphates in blood and urine is a marker of renal pathology." Problems of Uninterrupted Medical Training and Science 2017, no. 1 (April 2017): 58–61. http://dx.doi.org/10.31071/promedosvity2017.01.058.

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8

Borda, Enri, Graciela Stranieri, and Leonor Sterin-Borda. "H1-Receptor activation triggers the endogenous nitric oxide signalling system in the rat submandibular gland." Mediators of Inflammation 11, no. 6 (2002): 337–43. http://dx.doi.org/10.1080/0962935021000051520.

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Background: Histamine is released from mast cells by immunologic and non-immunologic stimuli during salivary gland inflammation, regulating salivary secretion. The receptor-secretory mechanism has not been studied in detail.Aims: The studies reported were directed toward elucidating signal transduction/second messenger pathways within the rat submandibular gland associated with 2-thiazolylethylamine (ThEA)-induced H1-receptor responses.Materials and methods: To assess the H1receptor subtype expression in the rat submandibular gland, a radioligand binding assay was performed. The study also included inositolphosphates and cyclic GMP accumulation, protein kinase C and nitric oxide synthase activities, and amylase release.Results: The histamine H1receptor subtype is expressed on the rat submandibular gland with high-affinity binding sites. The ThEA effect was associated with activation of phosphoinositide-specific phospholipase C, translocation of protein kinase C, stimulation of nitric oxide synthase activity and increased production of cyclic GMP. ThEA stimulation of nitric oxide synthase and cyclic GMP was blunted by agents able to interfere with calcium movilization, while a protein kinase C inhibitor was able to stimulate ThEA action. On the other hand, ThEA stimulation evoked amylase release via the H1receptor but was not followed by the L-arginine/nitric oxide pathway activation.Conclusions: These results suggest that, apart from the effect of ThEA on amylase release, it also appears to be a vasoactive chemical mediator that triggers vasodilatation, modulating the course of inflammation.

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9

Ticchioni, M., C. Aussel, J. P. Breittmayer, S. Manié, C. Pelassy, and A. Bernard. "Suppressive effect of T cell proliferation via the CD29 molecule. The CD29 mAb 1 "K20" decreases diacylglycerol and phosphatidic acid levels in activated T cells." Journal of Immunology 151, no. 1 (July 1, 1993): 119–27. http://dx.doi.org/10.4049/jimmunol.151.1.119.

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Abstract We had previously reported that the CD29 mAb "K20," presented in a soluble form, blocks peripheral T cell proliferation/activation induced by a CD3 mAb. To better characterize the negative signal delivered by soluble K20, we have investigated its effects on the phospholipid metabolism, both in Jurkat and CD4+ T cells. In CD3-activated T cells, K20 inhibited the increase of diacylglycerol (DAG) and phosphatidic acid levels, but did not modify phosphatidylinositol 4,5-bisphosphate levels, cytosolic Ca2+ raise, and inositolphosphates formation, indicating that K20 did not inhibit phosphatidylinositol 4,5-bisphosphate hydrolysis by phospholipase C-gamma. Moreover, in these conditions, K20 increased phosphatidylethanolamine levels, without variation of phosphatidylcholine, phosphatidylserine, and phosphatidylinositol, suggesting that K20 specifically increased the phosphatidylethanolamine biosynthesis from DAG. Thus, the effects of K20 on DAG and phosphatidic acid levels resulted from an accelerated catabolism rather than from a defect of synthesis. That K20 acts solely at an early step of T cell activation, namely before the binding of IL-2 to its receptor, is supported by the observation that adding exogenous rIL-2 increased proliferation in spite of K20. These results suggest that the beta 1 integrin molecules interact with the membrane phospholipid metabolism and they appear to be the hallmark of a peculiar negative pathway of T cell activation, likely to play an important regulatory role mediated via the T cell integrin molecules.

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10

FRAGOSO, GABRIELA, and ANA MARÍA LÓPEZ-COLOMÉ. "Excitatory amino acid-induced inositol phosphate formation in cultured retinal pigment epithelium." Visual Neuroscience 16, no. 2 (March 1999): 263–69. http://dx.doi.org/10.1017/s0952523899162072.

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Excitatory amino acid (EAA)-induced production of inositolphosphates (IPs) was studied in primary cultures of chick retinal pigment epithelium (RPE) following in vitro incorporation of [3H] myo-inositol. Glutamic acid (L-glu) significantly increased [3H]-IPs accumulation (215%). L-glu agonists stimulated [3H]IPs accumulation in the following order of efficiency: N-methyl-D-aspartate (NMDA) ≥ L-glu > quisqualate ≥ kainate > (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD). Stimulation was dependent on external Ca2+. The NMDA-induced response was blocked by (+)-5-methyl-10,11-dihydro-5H-dibenzo-cyclohepten-5,10-imine maleate (MK-801) and 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and was decreased by the L-Ca2+-channel blockers verapamil and nifedipine as well as by dantrolene. The metabotropic glutamate receptor (mGluR) antagonist (+)-α-methyl-4-carboxyphenylglycine (+)MCPG inhibited 3,5-dihydroxyphenylglycine (DHPG) and ACPD-induced stimulation, which demonstrates the presence in RPE of mGluRs 1 and/or 5, as well as NMDA receptors coupled directly, or through the influx of external Ca2+, to phospholipase C activation. L-glu agonists showed no effect either on basal level of intracellular cyclic adenosine monophosphate, nor on forskolin- or carbachol-induced stimulation of adenylyl cyclase. Since L-glu is released from the retina upon illumination, and receptors for this compound are present in RPE, the activation of the inositide pathway could be involved in the regulation of retina-RPE interaction, which is essential for the visual process.

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11

Bjøro, T., K. Englund, P. A. Torjesen, and E. Haug. "Inhibitors of the arachidonic acid metabolism attenuate the thyroliberin (TRH) stimulated prolactin production without modifying the production of inositolphosphates in GH4C1pituitary cells." Scandinavian Journal of Clinical and Laboratory Investigation 53, no. 2 (January 1993): 111–16. http://dx.doi.org/10.3109/00365519309088397.

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12

Nakaki, Toshio, Nobuyuki Sasakawa, Satoshi Yamamoto, and Ryuichi Kato. "Changes in receptor-mediated signal transduction systems from muscarinic to nicotinic receptors that are coupled to generation of inositolphosphates in adrenal chromaffin cells." Japanese Journal of Pharmacology 43 (1987): 164. http://dx.doi.org/10.1016/s0021-5198(19)58297-x.

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13

Cunningham, Earlene Brown. "An Inositolphosphate-Binding Immunophilin, IPBP12." Blood 94, no. 8 (October 15, 1999): 2778–89. http://dx.doi.org/10.1182/blood.v94.8.2778.420k10_2778_2789.

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A novel inositolphosphate-binding protein has been identified and shown to be an immunophilin. This protein, which was isolated from human erythrocyte membranes and from K562 (human erythroleukemia) cell membranes, has robust peptidylprolyl cis-trans isomerase activity that is strongly inhibited by nanomolar concentrations of FK506 or rapamycin, indicating a member of the FKBP (FK506-binding protein) class. However, unlike the cytosolic FKBP12, the isomerase activity of this membrane-associated immunophilin is strongly inhibited by nanomolar concentrations of inositol 1,4,5-trisphosphate (IP3), inositol 1,3,4,5-tetrakisphosphate (IP4), and phosphatidylinositol 4- and 4,5-phosphates, which are suggested to be physiological ligands. The demonstration of a single 12-kD protein that binds both IP4 or IP3and anti-FKBP12 provides strong support for the inositolphosphate-binding immunophilin having an apparent mass of 12 kD, and it is suggested that the protein might be called IPBP12 for 12-kD inositol phosphate binding protein. When an internal tryptic peptide derived from IPBP12 was sequenced, a sequence also present in human cytokeratin 10 was identified, suggesting a cytoskeletal localization for the immunophilin. While purifying IPBP12, it was found that it is immunoprecipitated with specific proteins that include a protein kinase and a phosphoprotein phosphatase. The latter is indicated to be phosphoprotein phosphatase 2A (PP-2A). It is suggested that immunophilins promote the assembly of multiprotein complexes that often include a protein kinase or a phosphoprotein phosphatase or both.

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14

Rao, R. K., and C. V. Ramakrishnan. "Studies on Inositolphosphatase in Rat Small Intestine." Enzyme 33, no. 4 (1985): 205–15. http://dx.doi.org/10.1159/000469435.

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15

Garg, Jaspal, Alexandra Sporkova, Markus Hecker, and Thomas Korff. "Tracing G-Protein-Mediated Contraction and Relaxation in Vascular Smooth Muscle Cell Spheroids." Cells 12, no. 1 (December 28, 2022): 128. http://dx.doi.org/10.3390/cells12010128.

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Analyses of G-protein-mediated contraction and relaxation of vascular smooth muscle cells (VSMCs) are usually hampered by a rigid growth surface and culture conditions promoting cell proliferation and a less contractile phenotype. Our studies indicated that mouse aortic VSMCs cultured in three-dimensional spheroids acquire a quiescent contractile status while decreasing the baseline G-protein-dependent inositolphosphate formation and increasing the expression of endothelin receptor type A (Ednra). Endothelin-1 (ET-1) promoted inositolphosphate formation in VSMC spheroids, but not in VSMCs cultured under standard conditions. To trace ET-1-mediated contraction of VSMC spheroids, we developed an assay by adhering them to collagen hydrogels and recording structural changes by time-lapse microscopy. Under these conditions, mouse and human VSMC spheroids contracted upon treatment with ET-1 and potassium chloride or relaxed in response to caffeine and the prostacyclin analogue Iloprost. ET-1 activated AKT-, MKK1-, and MKK3/6-dependent signaling cascades, which were inhibited by an overexpressing regulator of G-protein signaling 5 (Rgs5) to terminate the activity of Gα subunits. In summary, culture of VSMCs in three-dimensional spheroids lowers baseline G-protein activity and enables analyses of both contraction and relaxation of mouse and human VSMCs. This model serves as a simple and versatile tool for drug testing and investigating G-protein-depending signaling.

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16

Scholz, J., N. Roewer, U. Troll, M. Patten, W. Schmitz, H. Scholz, and J. Schulte am Esch. "Maligne Hyperthermie und Inositolphosphat-Stoffwechsel in Herz- und Skelettmuskulatur." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 26, no. 08 (December 1991): 450–53. http://dx.doi.org/10.1055/s-2007-1000614.

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17

Tandon, P., C. Pope, S. Padilla, H. A. Tilson, and G. J. Harry. "Developmental changes in carbachol-stimulated inositolphosphate release in pigmented rat retina." Current Eye Research 12, no. 5 (January 1993): 439–49. http://dx.doi.org/10.3109/02713689309024626.

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18

Habermann, E., and M. Laux. "Depolarization increases inositolphosphate production in a particulate preparation from rat brain." Naunyn-Schmiedeberg's Archives of Pharmacology 334, no. 1 (September 1986): 1–9. http://dx.doi.org/10.1007/bf00498733.

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19

Jansen, I., J. You, and L. Edvinsson. "α-trinositol blocks neuropeptide Y-induced inositolphosphate formation in cerebral vessels." Neuropeptides 26, no. 5 (May 1994): 305–12. http://dx.doi.org/10.1016/0143-4179(94)90115-5.

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20

Teng, Che-Ming, Lin Chun-Nan, Ko Feng-Nien, Cheng Kam-Lin, and Huang Tur-Fu. "Novel inhibitory actions on platelet thromboxane and inositolphosphate formation by xanthones and their glycosides." Biochemical Pharmacology 38, no. 21 (November 1989): 3791–95. http://dx.doi.org/10.1016/0006-2952(89)90587-x.

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21

Devemy, Emmanuelle, Claudnie Billat, Herve Sartelet, Laurent Martiny, and Bernard Haye. "Erythropoietin stimulates glycosylphosphatidylinositol hydrolisis in rat erythroid progenitor cells and inositolphosphate glycan modulates their proliferation." Cellular Signalling 6, no. 5 (July 1994): 523–29. http://dx.doi.org/10.1016/0898-6568(94)90006-x.

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22

Vivien, Denis, Emmanuelle Petitfrère, Laurent Martiny, Hervè Sartelet, Philippe Galéra, Bernard Haye, and Jean-Pierre Pujol. "IPG (inositolphosphate glycan) as a cellular signal for TGF-β1 modulation of chondrocyte cell cycle." Journal of Cellular Physiology 155, no. 3 (June 1993): 437–44. http://dx.doi.org/10.1002/jcp.1041550302.

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23

Dhein, Stefan, Christine Giessler, Karin Becker, Klaus Pönicke, and Otto-Erich Brodde. "Inositolphosphate formation in thoracic and abdominal rat aorta following G q/11 -coupled receptor stimulation." Naunyn-Schmiedeberg's Archives of Pharmacology 363, no. 3 (February 14, 2001): 322–29. http://dx.doi.org/10.1007/s002100000344.

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24

Biber, Knut, Jörg Walden, Peter Gebicke-Härter, Mathias Berger, and Dietrich van Calker. "Carbamazepine inhibits the potentiation by adenosine analogues of agonist induced inositolphosphate formation in hippocampal astrocyte cultures." Biological Psychiatry 40, no. 7 (October 1996): 563–67. http://dx.doi.org/10.1016/0006-3223(96)00031-5.

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25

Webb, Kimberly M., and Jocelyne DiRuggiero. "Role of Mn2+and Compatible Solutes in the Radiation Resistance of Thermophilic Bacteria and Archaea." Archaea 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/845756.

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Radiation-resistant bacteria have garnered a great deal of attention from scientists seeking to expose the mechanisms underlying their incredible survival abilities. Recent analyses showed that the resistance to ionizing radiation (IR) in the archaeonHalobacterium salinarumis dependent upon Mn-antioxidant complexes responsible for the scavenging of reactive oxygen species (ROS) generated by radiation. Here we examined the role of the compatible solutes trehalose, mannosylglycerate, anddi-myo-inositolphosphate in the radiation resistance of aerobic and anaerobic thermophiles. We found that the IR resistance of the thermophilic bacteriaRubrobacter xylanophilusandRubrobacter radiotoleranswas highly correlated to the accumulation of high intracellular concentration of trehalose in association with Mn, supporting the model of Mn2+-dependent ROS scavenging in the aerobes. In contrast, the hyperthermophilic archaeaThermococcus gammatoleransandPyrococcus furiosusdid not contain significant amounts of intracellular Mn, and we found no significant antioxidant activity from mannosylglycerate and di-myo-inositol phosphatein vitro. We therefore propose that the low levels of IR-generated ROS under anaerobic conditions combined with highly constitutively expressed detoxification systems in these anaerobes are key to their radiation resistance and circumvent the need for the accumulation of Mn-antioxidant complexes in the cell.

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26

Higashida, Haruhiro. "Bradykinin-Evoked Inositolphosphate/Calcium-Dependent Responses and Potassium Channels in Neuroblastoma x Glioma Hybrid NG108-15 Cells." Japanese Journal of Pharmacology 61 (1993): 46. http://dx.doi.org/10.1016/s0021-5198(19)51147-7.

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27

Petitfrere, Emmanuelle, Herve Sartelet, Denis Vivien, Isabel Varela-Nieto, Hassan Elbtaouri, Laurent Martiny, and Bernard Haye. "Glycosyl phosphatidylinositol (GPI)/inositolphosphate glycan (GPI): An intracellular signalling system involved in the control of thyroid cell proliferation." Biochimie 80, no. 12 (December 1998): 1063–67. http://dx.doi.org/10.1016/s0300-9084(99)80013-3.

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28

Her, E., N. Reiss, P. Braquet, and U. Zor. "Characterization of glucocorticoid inhibition of antigen-induced inositolphosphate formation by rat basophilic leukemia cells: possible involvement of phosphatases." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1133, no. 1 (December 1991): 63–72. http://dx.doi.org/10.1016/0167-4889(91)90242-p.

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29

Los, Georgyi V., Irina P. Artemenko, and Lowell E. Hokin. "Phosphoinositide signalling in human neuroblastoma cells: Biphasic effect of Li+ on the level of the inositolphosphate second messengers." Advances in Enzyme Regulation 36 (January 1996): 245–64. http://dx.doi.org/10.1016/0065-2571(95)00022-4.

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30

VIVIEN, D., P. BOGDANOWICZ, K. BOUMEDIENE, L. MARTINY, B. HAYE, and J. PUJOL. "Different phosphorylated forms of inositolphosphate glycan could be involved in the transforming growth factor-gb 1 (TGF-β1) signalling pathway." Cellular Signalling 6, no. 2 (February 1994): 173–80. http://dx.doi.org/10.1016/0898-6568(94)90074-4.

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31

Vollenweider, Peter, Martin Clodi, Stuart S. Martin, Takeshi Imamura, W. Michael Kavanaugh, and Jerrold M. Olefsky. "An SH2 Domain-Containing 5′ Inositolphosphatase Inhibits Insulin-Induced GLUT4 Translocation and Growth Factor-Induced Actin Filament Rearrangement." Molecular and Cellular Biology 19, no. 2 (February 1, 1999): 1081–91. http://dx.doi.org/10.1128/mcb.19.2.1081.

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ABSTRACT Tyrosine kinase receptors lead to rapid activation of phosphatidylinositol 3-kinase (PI3 kinase) and the subsequent formation of phosphatidylinositides (PtdIns) 3,4-P2 and PtdIns 3,4,5-P3, which are thought to be involved in signaling for glucose transporter GLUT4 translocation, cytoskeletal rearrangement, and DNA synthesis. However, the specific role of each of these PtdIns in insulin and growth factor signaling is still mainly unknown. Therefore, we assessed, in the current study, the effect of SH2-containing inositol phosphatase (SHIP) expression on these biological effects. SHIP is a 5′ phosphatase that decreases the intracellular levels of PtdIns 3,4,5-P3. Expression of SHIP after nuclear microinjection in 3T3-L1 adipocytes inhibited insulin-induced GLUT4 translocation by 100 ± 21% (mean ± the standard error) at submaximal (3 ng/ml) and 64 ± 5% at maximal (10 ng/ml) insulin concentrations (P < 0.05 and P < 0.001, respectively). A catalytically inactive mutant of SHIP had no effect on insulin-induced GLUT4 translocation. Furthermore, SHIP also abolished GLUT4 translocation induced by a membrane-targeted catalytic subunit of PI3 kinase. In addition, insulin-, insulin-like growth factor I (IGF-I)-, and platelet-derived growth factor-induced cytoskeletal rearrangement, i.e., membrane ruffling, was significantly inhibited (78 ± 10, 64 ± 3, and 62 ± 5%, respectively; P < 0.05 for all) in 3T3-L1 adipocytes. In a rat fibroblast cell line overexpressing the human insulin receptor (HIRc-B), SHIP inhibited membrane ruffling induced by insulin and IGF-I by 76 ± 3% (P < 0.001) and 68 ± 5% (P < 0.005), respectively. However, growth factor-induced stress fiber breakdown was not affected by SHIP expression. Finally, SHIP decreased significantly growth factor-induced mitogen-activated protein kinase activation and DNA synthesis. Expression of the catalytically inactive mutant had no effect on these cellular responses. In summary, our results show that expression of SHIP inhibits insulin-induced GLUT4 translocation, growth factor-induced membrane ruffling, and DNA synthesis, indicating that PtdIns 3,4,5-P3 is the key phospholipid product mediating these biological actions.

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32

Bogdanowicz, Patrick, Denis Vivien, Nathalie Felisaz, Vincent Léon, and Jean-Pierre Pujol. "An inositolphosphate glycan released by TGF-β mimics the proliferative but not the transcriptional effects of the factor and requires functional receptors." Cellular Signalling 8, no. 7 (November 1996): 503–9. http://dx.doi.org/10.1016/s0898-6568(96)00106-4.

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33

Donié, Frédéric, and Georg Reiser. "Mass measurements of inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate in a neuronal cell line stimulated with bradykinin: Inositolphosphate response shows desensitization." Biochemical and Biophysical Research Communications 181, no. 3 (December 1991): 997–1003. http://dx.doi.org/10.1016/0006-291x(91)92035-i.

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34

Devemy, Emmanuelle, Claudine Billat, and Bernard Haye. "Activation of Raf-1 and Mitogen-Activated Protein Kinases by Erythropoietin and Inositolphosphate-Glycan in Normal Erythroid Progenitor Cells: Involvement of Protein Kinase C." Cellular Signalling 9, no. 1 (January 1997): 41–46. http://dx.doi.org/10.1016/s0898-6568(96)00095-2.

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35

Safari, K., S. Menzies, H. Jung, and L. M. Sly. "A39 TARGETING IL-4 TO TREAT CROHN’S DISEASE ASSOCIATED INTESTINAL FIBROSIS IN SHIP DEFICIENT MICE." Journal of the Canadian Association of Gastroenterology 5, Supplement_1 (February 21, 2022): 46–47. http://dx.doi.org/10.1093/jcag/gwab049.038.

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Abstract Background Crohn’s disease (CD) is an immune-mediated disease characterized by chronic, relapsing, or progressive inflammation along the gastrointestinal tract. One in 3 people with CD will develop intestinal fibrosis requiring surgery within 10 years of diagnosis. Biological therapy is very effective at reducing inflammation in CD; however, biologics do not reduce the incidence of fibrosis or surgery in people with CD, suggesting that a distinct mechanism(s) may exist that drives intestinal fibrosis. Treatments for intestinal fibrosis are urgently needed as currently, no treatment exists that target intestinal fibrosis directly. Mice deficient in the Src homology 2 domain-containing inositolphosphate 5’-phosphatase (SHIP-/-) develop spontaneous CD-like ileal inflammation and fibrosis. Fibrosis is dependent on PI3Kp110δ activation, which leads to induction of the enzyme arginase I (argI). Genetic ablation or pharmacologic inhibition of PI3Kp110δ or inhibition of arginase activity blocked the development of intestinal fibrosis in SHIP-/- mice. Both IL-4 and IL-13 can activate PI3Kp110δ but intestinal pathology in SHIP-/- mice is characterized by high levels of IL-4. Thus, we hypothesize that SHIP-/- mice develop CD-like intestinal fibrosis due to increased IL-4 signalling. Aims Aim 1: To determine whether genetic ablation of IL-4 prevents ileal fibrosis in SHIP-/- mice Aim 2 To determine whether inhibition of IL-4 activity can block or reverse ileal fibrosis in SHIP-/- mice Methods SHIP-/- mice were crossed with mice deficient in IL-4 (IL-4-/-) to generate wild type, SHIP+/+IL-4-/- SHIP-/-IL-4+/+, and SHIP-/-IL4-/- mice. Fibrosis was assessed in mice at 8 weeks of age. SHIP-/- mice (8-week-old) were treated with an anti-IL-4 antibody, IgG isotype control or PBS (injection control), for 2 weeks. Ileal fibrosis was assessed in SHIP-/- mice and compared to mice treated with anti-IL-4 antibody or controls. Measurements of ileal fibrosis include muscle thickening, and collagen accumulation by Masson’s trichrome staining. Results SHIP-/-IL4-/- mice do not have less ileal fibrosis than their SHIP-/- littermates. Inhibition of IL-4 signalling in SHIP-/- mice did not reduce ileal fibrosis. Conclusions Blocking IL-4 is not sufficient to block the development of ileal fibrosis in SHIP-/- mice. In future experiments, we will examine whether blocking IL-13, alone or in combination with IL-4, can ameliorate the development of intestinal fibrosis in SHIP-/- mice. Funding Agencies CIHR

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Kleineke, Jochen. "Aktuelles über Inositolphosphate: The Inositol Phosphates. Chemical Synthesis and Biological Significance. Von D. C. Billington. VCH Verlagsgesellschaft, Weinheim, 1993. 154 S., Abb., Tab., geb. DM 126,-. ISBN 3-527-28152-5." Nachrichten aus Chemie, Technik und Laboratorium 41, no. 10 (October 1993): 1158–60. http://dx.doi.org/10.1002/nadc.19930411026.

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"IPG (inositolphosphate glycan) as a cellular signal for TGFβ modulation of chondrocyte cell cycle." Osteoarthritis and Cartilage 1, no. 1 (January 1993): 26–27. http://dx.doi.org/10.1016/s1063-4584(05)80171-2.

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Hofmann, Fred, and Ernst Habermann. "Role of ?-conotoxin-sensitive calcium channels in inositolphosphate production and noradrenaline release due to potassium depolarization or stimulation with carbachol." Naunyn-Schmiedeberg's Archives of Pharmacology 341, no. 3 (March 1990). http://dx.doi.org/10.1007/bf00169731.

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Kofron, Celinda M., Tae Yun Kim, Michelle E. King, Elizabeth M. Park, Bum-Rak Choi, and Ulrike Mende. "Abstract 16606: Cardiac Fibroblast-Restricted Enhancement of G q Signaling Prolongs Calcium Transients and Increases Spontaneous Activity in Biomimetic Cardiac Microtissues." Circulation 130, suppl_2 (November 25, 2014). http://dx.doi.org/10.1161/circ.130.suppl_2.16606.

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Introduction: Enhanced G q signaling in response to hemodynamic stress and injury is well known to induce remodeling in both cardiac myocytes (CMs) and fibroblasts (CFs). However, the effect of CF activation and fibrosis on CMs and integrated myocardial function cannot be easily discerned from concomitant effects on CMs. Hypothesis: Enhanced G q signaling in CFs influences CM function in a 3D microtissue model previously developed in our lab, in which neonatal rat ventricular CMs and CFs are highly interspersed as seen in the myocardium. Methods: CFs infected in suspension (2 hrs, 10 MOI) with empty adenovirus (Ad-Ctr) or Ad encoding wild-type (WT) or constitutively active (Q209L or QL) Gα q were co-seeded with uninfected CMs (CM:CF 1:1) into non-adhesive hydrogels at ~1200 cells per recess (400/800 μm wide/deep). After 2-4 days, we assessed tissue size by microscopy, G q and extracellular matrix proteins proteins by Western Blot analysis, and Ca 2+ transients ([Ca 2+ ] i ) with Rhod 2/AM. Results: Overexpression of Gα q in CFs was associated with a 3-fold (WT) and 7-fold (QL) increase in total inositolphosphate formation, indicating enhanced basal phospholipase β activity. After 4 days, CM:CF QL tissues were larger in size by 30-40% and expressed more laminin and fibronectin. After 3 days, CM:CF CTR paced at 1 Hz had [Ca 2+ ] i duration of 218±3 ms, decay of 141±2 ms, and rise time of 35±4 ms (n=55-69). In CM:CF QL , duration and decay were prolonged by 160 ms and 21 ms, resp., and rise time was decreased by 5 ms (n=10-27). In CM:CF WT with less G q signaling, [Ca 2+ ] i duration and decay were also prolonged but only by 30 ms and 7 ms, resp. (n=46-51). These effects were similar but less pronounced after 2 days and/or at 2 Hz. Spontaneous [Ca 2+ ] i activity was seen in 50% of CM:CF QL , 11% of CM:CF WT , but only 2% of CM:CF CTR microtissues. The gap junction inhibitor carbenoxolone (100 μM) decreased this activity in CM:CF QL by 80% and in CM:CF WT by 15%. Conclusion: We show that enhanced CF-restricted G q signaling in biomimetic cardiac microtissues increases tissue size, prolongs [Ca 2+ ] i duration and decay, and increases spontaneous Ca 2+ activity. Our findings suggest that depending on the CF activation state, CFs can greatly modulate CM calcium handling and potentially influence arrhythmogenesis.

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