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Journal articles on the topic 'Tumor necrosis factor Physiological effect'

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Published: 4 June 2021

Last updated: 28 January 2023

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1

Todorov, Vladimir, Markus Müller, Frank Schweda та Armin Kurtz. "Tumor necrosis factor-α inhibits renin gene expression". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, № 5 (1 листопада 2002): R1046—R1051. http://dx.doi.org/10.1152/ajpregu.00142.2002.

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Renin, produced in renal juxtaglomerular (JG) cells, is a fundamental regulator of blood pressure. Accumulating evidence suggests that cytokines may directly influence renin production in the JG cells. TNF-α, which is one of the key mediators in immunity and inflammation, is known to participate in the control of vascular proliferation and contraction and hence in the pathogenesis of cardiovascular diseases. Thus TNF-α may exert its effects on the cardiovascular system through modulation of renal renin synthesis. Therefore we have tested the effect of TNF-α on renin transcription in As4.1 cell

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Greenberg, S., J. Xie, Y. Wang, B. Cai, J. Kolls, S. Nelson, A. Hyman, W. R. Summer, and H. Lippton. "Tumor necrosis factor-alpha inhibits endothelium-dependent relaxation." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2394–403. http://dx.doi.org/10.1152/jappl.1993.74.5.2394.

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Tumor necrosis factor-alpha (TNF-alpha) stimulates nitric oxide (NO) in vascular endothelium by induction of the enzyme NO synthase II (NOS II). We examined the effects of TNF-alpha on 1) endothelium-dependent (EDR) and endothelium-independent (EIR) relaxation and 2) contraction of bovine intralobar pulmonary arteries (BPA) and veins (BPV) in vitro. Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-

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Moller, A. D., and P. O. Grande. "Low-dose prostacyclin has potent capillary permeability-reducing effect in cat skeletal muscle in vivo." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (July 1, 1997): H200—H207. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h200.

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The dose-response effects of intravenous infusion of prostacyclin on capillary permeability (the capillary filtration coefficient technique), hydrostatic capillary pressure, transcapillary filtration, and vascular tone were analyzed in vivo on cat skeletal muscle from a normal and an increased permeability level. Increased permeability was accomplished by intra-arterial infusion of tumor necrosis factor-alpha or histamine. Permeability effects of bradykinin were also analyzed. Prostacyclin decreased capillary permeability by 8% at a dose of 0.1 ng.kg-1.min-1 and at most by 30% below control at

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4

Alexander, H. R., G. G. Wong, G. M. Doherty, D. J. Venzon, D. L. Fraker, and J. A. Norton. "Differentiation factor/leukemia inhibitory factor protection against lethal endotoxemia in mice: synergistic effect with interleukin 1 and tumor necrosis factor." Journal of Experimental Medicine 175, no. 4 (April 1, 1992): 1139–42. http://dx.doi.org/10.1084/jem.175.4.1139.

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Differentiation factor (D factor), also called leukemia inhibitory factor (LIF), is a glycoprotein that has been increasingly recognized to possess a wide range of physiological activities. We examined the possibility that the administration of D factor may confer beneficial effects and enhance host resistance against lethal endotoxemia. A single intravenous dose of recombinant human D factor completely protected C57/Bl6 mice from the lethal effect of Escherichia coli endotoxin (lipopolysaccharide [LPS]). The protective effects were dose dependent and observed when administered 2-24 h before L

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Takahashi, Satoshi, Levente Kapás, Jidong Fang, and James M. Krueger. "Somnogenic relationships between tumor necrosis factor and interleukin-1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 4 (April 1, 1999): R1132—R1140. http://dx.doi.org/10.1152/ajpregu.1999.276.4.r1132.

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Both tumor necrosis factor (TNF) and interleukin (IL)-1 are somnogenic cytokines. They also induce each other’s production and both induce nuclear factor kappa B activation, which in turn enhances IL-1 and TNF transcription. We hypothesized that TNF and IL-1 could influence each other’s somnogenic actions. To test this hypothesis, we determined the effects of blocking both endogenous TNF and IL-1 on spontaneous sleep and on sleep rebound after sleep deprivation in rabbits. Furthermore, the effects of inhibition of TNF on IL-1-induced sleep and the effects of blocking IL-1 on TNF-induced sleep

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Tseng, Wei-Cheng, Hou-Chuan Lai, Yi-Hsuan Huang, Shun-Ming Chan, and Zhi-Fu Wu. "Tumor Necrosis Factor Alpha: Implications of Anesthesia on Cancers." Cancers 15, no. 3 (January 25, 2023): 739. http://dx.doi.org/10.3390/cancers15030739.

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Cancer remains a major public health issue and a leading cause of death worldwide. Despite advancements in chemotherapy, radiation therapy, and immunotherapy, surgery is the mainstay of cancer treatment for solid tumors. However, tumor cells are known to disseminate into the vascular and lymphatic systems during surgical manipulation. Additionally, surgery-induced stress responses can produce an immunosuppressive environment that is favorable for cancer relapse. Up to 90% of cancer-related deaths are the result of metastatic disease after surgical resection. Emerging evidence shows that the in

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7

Ramseyer, Vanesa D., та Jeffrey L. Garvin. "Tumor necrosis factor-α: regulation of renal function and blood pressure". American Journal of Physiology-Renal Physiology 304, № 10 (15 травня 2013): F1231—F1242. http://dx.doi.org/10.1152/ajprenal.00557.2012.

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Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that becomes elevated in chronic inflammatory states such as hypertension and diabetes and has been found to mediate both increases and decreases in blood pressure. High levels of TNF-α decrease blood pressure, whereas moderate increases in TNF-α have been associated with increased NaCl retention and hypertension. The explanation for these disparate effects is not clear but could simply be due to different concentrations of TNF-α within the kidney, the physiological status of the subject, or the type of stimulus initiating the inflammat

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8

Salama, Salama A., Marwa W. Kamel, Concepcion R. Diaz-Arrastia, Xia Xu, Timothy D. Veenstra, Sana Salih, Shaleen K. Botting та Raj Kumar. "Effect of Tumor Necrosis Factor-α on Estrogen Metabolism and Endometrial Cells: Potential Physiological and Pathological Relevance". Journal of Clinical Endocrinology & Metabolism 94, № 1 (1 січня 2009): 285–93. http://dx.doi.org/10.1210/jc.2008-1389.

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9

Wang, Chen, Yuchen Wang, Na Liu, Chuan Cai та Lulu Xu. "Effect of tumor necrosis factor α on ability of SHED to promote osteoclastogenesis during physiological root resorption". Biomedicine & Pharmacotherapy 114 (червень 2019): 108803. http://dx.doi.org/10.1016/j.biopha.2019.108803.

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10

Matsumoto, Yutaka, Yohko Kawai, Kiyoaki Watanabe, Kazuo Sakai, Mitsuru Murata, Makoto Handa, Shin Nakamura та Yasuo Ikeda. "Fluid Shear Stress Attenuates Tumor Necrosis Factor-α–Induced Tissue Factor Expression in Cultured Human Endothelial Cells". Blood 91, № 11 (1 червня 1998): 4164–72. http://dx.doi.org/10.1182/blood.v91.11.4164.

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Abstract Hemodynamic forces modulate various endothelial cell functions under gene regulation. Previously, we have shown that fibrinolytic activity of endothelial cells is enhanced by the synergistic effects of shear stress and cytokines. In this study, we investigated the effect of shear stress on tumor necrosis factor (TNF)-α–induced tissue factor (TF) expression in cultured human umbilical vein endothelial cells (HUVECs), using a modified cone-plate viscometer. Shear stresses at physiological levels reduced TNF-α (100 U/mL)–induced TF expression at both mRNA and antigen levels, in a shear-i

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Matsumoto, Yutaka, Yohko Kawai, Kiyoaki Watanabe, Kazuo Sakai, Mitsuru Murata, Makoto Handa, Shin Nakamura та Yasuo Ikeda. "Fluid Shear Stress Attenuates Tumor Necrosis Factor-α–Induced Tissue Factor Expression in Cultured Human Endothelial Cells". Blood 91, № 11 (1 червня 1998): 4164–72. http://dx.doi.org/10.1182/blood.v91.11.4164.411k29_4164_4172.

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Hemodynamic forces modulate various endothelial cell functions under gene regulation. Previously, we have shown that fibrinolytic activity of endothelial cells is enhanced by the synergistic effects of shear stress and cytokines. In this study, we investigated the effect of shear stress on tumor necrosis factor (TNF)-α–induced tissue factor (TF) expression in cultured human umbilical vein endothelial cells (HUVECs), using a modified cone-plate viscometer. Shear stresses at physiological levels reduced TNF-α (100 U/mL)–induced TF expression at both mRNA and antigen levels, in a shear-intensity

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Moxey-Mims, M. M., H. H. Simms, M. M. Frank, E. Y. Lin, and T. A. Gaither. "The effects of IL-1, IL-2, and tumor necrosis factor on polymorphonuclear leukocyte Fc gamma receptor-mediated phagocytosis. IL-2 down-regulates the effect of tumor necrosis factor." Journal of Immunology 147, no. 6 (September 15, 1991): 1823–30. http://dx.doi.org/10.4049/jimmunol.147.6.1823.

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Abstract It has been reported that the Fc gamma R-mediated phagocytic activity of polymorphonuclear leukocytes (PMN) from patients with acute bacterial infections is markedly enhanced when compared with healthy controls. Inasmuch as several potent cytokines are known to be involved in inflammatory and infectious processes, we studied the effects of three such cytokines (IL-1 beta, IL-2, and TNF-alpha) on normal PMN Fc gamma R-mediated phagocytosis. IL-1 beta and TNF alpha both caused a significant increase in the ingestion of EIgG by adherent PMN. In combination, IL-1 beta and TNF-alpha had an

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Tachimoto, Hiroshi, and Motohiro Ebisawa. "Effect of Interleukin-13 or Tumor Necrosis Factor-Alpha on Eosinophil Adhesion to Endothelial Cells under Physiological Flow Conditions." International Archives of Allergy and Immunology 143, no. 1 (2007): 33–37. http://dx.doi.org/10.1159/000101402.

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14

Alpini, Gianfranco, Yoshiyuki Ueno, Laura Tadlock, Shannon S. Glaser, Gene LeSage, Heather Francis, Silvia Taffetani, Marco Marzioni, Domenico Alvaro та Tushar Patel. "Increased susceptibility of cholangiocytes to tumor necrosis factor-α cytotoxicity after bile duct ligation". American Journal of Physiology-Cell Physiology 285, № 1 (липень 2003): C183—C194. http://dx.doi.org/10.1152/ajpcell.00497.2002.

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Tumor necrosis factor (TNF)-α plays a critical role in epithelial cell injury. However, the role of TNF-α in mediating cholangiocyte injury under physiological or pathophysiological conditions is unknown. Thus we assessed the effects of TNF-α alone or following sensitization by actinomycin D on cell apoptosis, proliferation, and basal and secretin-stimulated ductal secretion in cholangiocytes from normal or bile duct-ligated (BDL) rats. Cholangiocytes from normal or BDL rats were highly resistant to TNF-α alone. However, presensitization by actinomycin D increased apoptosis in cholangiocytes f

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Markova, T. N., N. K. Mishchenko, and D. V. Petina. "Adipocytokines: modern definition, classification and physiological role." Problems of Endocrinology 68, no. 1 (December 6, 2021): 73–80. http://dx.doi.org/10.14341/probl12805.

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Adipose tissue is an endocrine organ which produces a large number of secretory bioactive substances also known as adipocytokines affecting directly insulin resistance (IR), glucose and lipid metabolism, angiogenesis and inflammation. The studies show a close connection between the imbalance of adipocytokines formed as a result of excessive deposit of adipose tissue in the course of the development of type 2 diabetes mellitus and cardiovascular diseases. In the present review, we summarize current data on the effect of the adipocytokines on the liver, skeletal muscles, adipose tissue, endothel

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Guarnieri, Giulia, Erica Sarchielli, Paolo Comeglio, Erika Herrera-Puerta, Irene Piaceri, Benedetta Nacmias, Matteo Benelli та ін. "Tumor Necrosis Factor α Influences Phenotypic Plasticity and Promotes Epigenetic Changes in Human Basal Forebrain Cholinergic Neuroblasts". International Journal of Molecular Sciences 21, № 17 (25 серпня 2020): 6128. http://dx.doi.org/10.3390/ijms21176128.

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TNFα is the main proinflammatory cytokine implicated in the pathogenesis of neurodegenerative disorders, but it also modulates physiological functions in both the developing and adult brain. In this study, we investigated a potential direct role of TNFα in determining phenotypic changes of a recently established cellular model of human basal forebrain cholinergic neuroblasts isolated from the nucleus basalis of Meynert (hfNBMs). Exposing hfNBMs to TNFα reduced the expression of immature markers, such as nestin and β-tubulin III, and inhibited primary cilium formation. On the contrary, TNFα inc

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Ravid, A., E. Rubinstein, A. Gamady, C. Rotem, UA Liberman, and R. Koren. "Vitamin D inhibits the activation of stress-activated protein kinases by physiological and environmental stresses in keratinocytes." Journal of Endocrinology 173, no. 3 (June 1, 2002): 525–32. http://dx.doi.org/10.1677/joe.0.1730525.

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In addition to its known effects on keratinocyte proliferation and differentiation, the hormonal form of vitamin D, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), has been shown to protect keratinocytes from UV- and chemotherapy-induced damage. Epidermal keratinocytes contain both the machinery needed to produce 1,25(OH)(2)D(3) and vitamin D receptors. The activation of the stress-activated protein kinases (SAPKs), such as c-Jun N-terminal kinase (JNK) and p38, is an early cellular response to stress signals and an important determinant of cell fate. This study examines whether modulation of th

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18

Pan, Weihong, Germaine Cornélissen, Franz Halberg та Abba J. Kastin. "Selected Contribution: Circadian rhythm of tumor necrosis factor-α uptake into mouse spinal cord". Journal of Applied Physiology 92, № 3 (1 березня 2002): 1357–62. http://dx.doi.org/10.1152/japplphysiol.00915.2001.

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Circadian variations in the actions of tumor necrosis factor-α (TNF-α) have been observed. Because a saturable transport system at the blood-brain barrier mediates most of the influx of TNF-α from blood to the central nervous system (CNS), the circadian variation of the CNS effects of TNF-α could be related to changes in this transport system. Accordingly, we measured the uptake of intravenously injected TNF-α into various CNS regions at different times and compared these measurements with the uptake into a peripheral control (muscle). We found that the spinal cord, but not the brain, showed a

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Otsuka, Y., K. Nagano, K. Nagano, K. Hori, J. Oh-ishi, H. Hayashi, N. Watanabe, and Y. Niitsu. "Inhibition of neutrophil migration by tumor necrosis factor. Ex vivo and in vivo studies in comparison with in vitro effect." Journal of Immunology 145, no. 8 (October 15, 1990): 2639–43. http://dx.doi.org/10.4049/jimmunol.145.8.2639.

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Abstract Coincubation of neutrophils with TNF inhibited the chemoattractant-directed migration of neutrophils under agarose and enhanced their migration in the multiwell chemotaxis chamber. To assess the physiological significance of these differing in vitro TNF effects, ex vivo and in vivo investigations were performed using animal models. Neutrophils from the peripheral blood of rabbits preadministered systemic TNF showed impaired ability to migrate toward chemoattractants in vitro. In addition, systemic TNF administration suppressed zymosan-activated plasma-induced local accumulation of leu

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Yokochi, T., A. Kusumi, N. Kido, Y. Kato, T. Sugiyama, N. Koide, G. Z. Jiang, K. Narita, and K. Takahashi. "Differential release of smooth-type lipopolysaccharide from Pseudomonas aeruginosa treated with carbapenem antibiotics and its relation to production of tumor necrosis factor alpha and nitric oxide." Antimicrobial Agents and Chemotherapy 40, no. 10 (October 1996): 2410–12. http://dx.doi.org/10.1128/aac.40.10.2410.

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Endotoxin release from Pseudomonas aeruginosa treated with cell wall-active carbapenem antibiotics and its effect on the production of tumor necrosis factor alpha and nitric oxide were examined. Treatment of bacteria with imipenem induced much lower levels of endotoxin release than treatment with meropenem. The endotoxin released was demonstrated to be of the smooth type and O-specific polysaccharide-rich. The exposure of the filtrates of P. aeruginosa treated with imipenem to physiologically relevant cells caused low-level production of tumor necrosis factor alpha and nitric oxide, while simi

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Wilson, Michael R., Michael E. Goddard, Kieran P. O'Dea, Sharmila Choudhury, and Masao Takata. "Differential roles of p55 and p75 tumor necrosis factor receptors on stretch-induced pulmonary edema in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 1 (July 2007): L60—L68. http://dx.doi.org/10.1152/ajplung.00284.2006.

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Ventilator-induced lung injury plays a crucial role in the outcome of patients with acute lung injury. Previous studies have shown a role for the cytokine tumor necrosis factor-α (TNF) in stretch-induced alveolar neutrophil recruitment, but the involvement of TNF in stretch-induced pulmonary edema is unclear. We investigated the effects of TNF through its individual p55 and p75 receptors on early pulmonary edema formation during high stretch ventilation, before neutrophil infiltration. Anesthetized wild-type or TNF receptor single/double knockout mice were ventilated with high tidal volume (∼3

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Kubota, Takeshi, Jidong Fang, Zhiwei Guan, Richard A. Brown та James M. Krueger. "Vagotomy attenuates tumor necrosis factor-α-induced sleep and EEG δ-activity in rats". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, № 4 (1 квітня 2001): R1213—R1220. http://dx.doi.org/10.1152/ajpregu.2001.280.4.r1213.

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Much evidence suggests that tumor necrosis factor-α (TNF-α) is involved in the regulation of physiological sleep. However, it remains unclear whether peripheral administration of TNF-α induces sleep in rats. Furthermore, the role of the vagus nerve in the somnogenic actions of TNF-α had not heretofore been studied. Four doses of TNF-α were administered intraperitoneally just before the onset of the dark period. The three higher doses of TNF-α (50, 100, and 200 μg/kg) dose dependently increased nonrapid eye movement sleep (NREMS), accompanied by increases in electroencephalogram (EEG) slow-wave

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Ensor, J. E., S. M. Wiener, K. A. McCrea, R. M. Viscardi, E. K. Crawford, and J. D. Hasday. "Differential effects of hyperthermia on macrophage interleukin-6 and tumor necrosis factor-alpha expression." American Journal of Physiology-Cell Physiology 266, no. 4 (April 1, 1994): C967—C974. http://dx.doi.org/10.1152/ajpcell.1994.266.4.c967.

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The pyrogenic cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) appear in the circulation during infections and injuries, but TNF-alpha and IL-6 are regulated differently in macrophages. We compared the effects of elevated temperatures within the usual febrile range on the expression of TNF-alpha and IL-6 in vitro in lipopolysaccharide (LPS)-stimulated human macrophages derived from peripheral blood monocytes (HuMoM phi). During an 18-h incubation at 37 degrees C with 5 ng/ml LPS, these cells released 5,030 +/- 1,460 pg TNF-alpha/10(6) cells (means +/- SE) and 1,380 +/

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Vilcek, J., V. J. Palombella, D. Henriksen-DeStefano, C. Swenson, R. Feinman, M. Hirai, and M. Tsujimoto. "Fibroblast growth enhancing activity of tumor necrosis factor and its relationship to other polypeptide growth factors." Journal of Experimental Medicine 163, no. 3 (March 1, 1986): 632–43. http://dx.doi.org/10.1084/jem.163.3.632.

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Tumor necrosis factor (TNF) is a monocyte-derived protein cytotoxic or cytostatic for some tumor cell lines. Here we show that highly purified E. coli-derived recombinant human TNF stimulated the growth of human FS-4 diploid fibroblasts. Stimulation of cell growth was demonstrable at a TNF concentration of 10 pg/ml (3 X 10(-13) M). Maximal stimulation was attained at TNF concentrations of 10 ng/ml (3 X 10(-10) M) or higher. Growth-stimulatory activity of TNF was inhibited by an mAb neutralizing the cytotoxic activity of TNF. Growth stimulation was not inhibited by another mAb specific for TNF,

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Slungaard, A., G. M. Vercellotti, G. Walker, R. D. Nelson, and H. S. Jacob. "Tumor necrosis factor alpha/cachectin stimulates eosinophil oxidant production and toxicity towards human endothelium." Journal of Experimental Medicine 171, no. 6 (June 1, 1990): 2025–41. http://dx.doi.org/10.1084/jem.171.6.2025.

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Eosinophils (EOs) participate in a variety of inflammatory states characterized by endothelial cell damage, such as vasculitis, pneumonitis, and endocarditis. We find that 100 U/ml TNF-alpha/cachectin (TNF), a concentration attainable in the blood of humans with parasitic infestations, stimulates highly purified populations of EOs to damage human umbilical vein endothelial cells (HUVEC), a model of human endothelium. This TNF-dependent EO cytotoxicity is strongly inhibited by heparin and methyprednisolone but unaffected by the platelet-activating factor antagonist BN52012 or scavengers of supe

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Kubota, Takeshi, Jidong Fang, Tetsuya Kushikata та James M. Krueger. "Interleukin-13 and transforming growth factor-β1 inhibit spontaneous sleep in rabbits". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, № 3 (1 вересня 2000): R786—R792. http://dx.doi.org/10.1152/ajpregu.2000.279.3.r786.

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Proinflammatory cytokines, including interleukin-1β and tumor necrosis factor-α are involved in physiological sleep regulation. Interleukin (IL)-13 and transforming growth factor (TGF)-β1 are anti-inflammatory cytokines that inhibit proinflammatory cytokines by several mechanisms. Therefore, we hypothesized that IL-13 and TGF-β1 could attenuate sleep in rabbits. Three doses of IL-13 (8, 40, and 200 ng) and TGF-β1 (40, 100, and 200 ng) were injected intracerebroventricularly 3 h after the beginning of the light period. In addition, one dose of IL-13 (200 ng) and one dose of TGF-β1 (200 ng) were

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Mogulevtseva, J. A., A. V. Mezentsev, and S. A. Bruskin. "Impact of Metalloproteinase 1 Deficiency Induced by Specific Small Hairpin RNA on the Physiological Effects of Tumor Necrosis Factor." Russian Journal of Genetics 54, no. 8 (August 2018): 960–66. http://dx.doi.org/10.1134/s1022795418080094.

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Amari, T., K. Kubo, T. Kobayashi, and M. Sekiguchi. "Effects of recombinant human superoxide dismutase on tumor necrosis factor-induced lung injury in awake sheep." Journal of Applied Physiology 74, no. 6 (June 1, 1993): 2641–48. http://dx.doi.org/10.1152/jappl.1993.74.6.2641.

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Tumor necrosis factor alpha (TNF) is a mediator of acute lung injury after endotoxemia, but the precise mechanism of TNF-induced lung injury remains unclear. To clarify the role of oxygen radicals, especially superoxide anion, in TNF-induced lung injury, we examined the effects of recombinant human superoxide dismutase (rhSOD; 4,200 U/mg) on lung physiological and biochemical changes after TNF infusion in awake sheep (n = 17). We prepared chronically instrumented sheep for lung lymph collection and hemodynamic monitoring. Recombinant human TNF (3.5 micrograms/kg iv) induced a biphasic response

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Qin, Wen, Zhuo Yang, Jiyong Yin, Di Chen, Junsheng Huo, Jingbo Wang, Liyuan Wang, and Qin Zhuo. "Effect Assessment of Aurantio-Obtusin on Novel Human Renal Glomerular Endothelial Cells Model Using a Microfluidic Chip." Nutrients 14, no. 21 (November 2, 2022): 4615. http://dx.doi.org/10.3390/nu14214615.

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Cassiae semen is widely used as a raw material of health food. Anthraquinone compounds, the main components in cassiae semen, have been reported to show nephrotoxicity. Aurantio-obtusin (AO) is a major anthraquinone compound extracted from cassiae semen. This study investigates the effects of AO on the morphology and physiological function of human renal glomerular endothelial cells (HRGECs) on a microfluidic chip device for the first time. HRGECs were cultured on a microfluidic plate and exposed to a series of AO concentrations. Compared with traditional 96-well culture, HRGECs cultured on th

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Pamir, Nathalie, Timothy S. McMillen, Karl J. Kaiyala, Michael W. Schwartz та Renée C. LeBoeuf. "Receptors for Tumor Necrosis Factor-α Play a Protective Role against Obesity and Alter Adipose Tissue Macrophage Status". Endocrinology 150, № 9 (28 травня 2009): 4124–34. http://dx.doi.org/10.1210/en.2009-0137.

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Abstract TNF-α signals through two receptors, TNFR1 and TNFR2. Our goals were: 1) determine the role of TNFRs in obesity and metabolic disease and 2) investigate whether TNFRs contribute to the link between obesity and adipose tissue macrophage infiltration and polarization. R1−/−R2−/− (RKO) and wild-type (WT) mice were fed standard chow or a high-fat/high-sucrose diet (HFHS) over 14 wk. Body composition, food intake, and energy expenditure were measured. Oral glucose tolerance and insulin sensitivity tests assessed glucose homeostasis. Adipose tissue and systemic inflammatory status were eval

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Lanuza, Guillermo M., Patricia E. Saragüeta, Ursula A. Bussmann та J. Lino Barañao. "Paradoxical effects of tumour necrosis factor-α on rat granulosa cell DNA synthesis". Reproduction, Fertility and Development 14, № 3 (2002): 133. http://dx.doi.org/10.1071/rd01103.

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Tumour necrosis factor- α (TNF-α ) has been proposed as an intraovarian modulator of granulosa cell function. The effect of TNF-α on DNA synthesis in cultured rat granulosa cells was examined. Tumour necrosis factor-α stimulated thymidine incorporation when added in the presence of transforming growth factor-β (TGF-β). In contrast, the co-mitogenic effect of follicle-stimulating hormone (FSH) and TGF-β was inhibited in a dose-dependent manner by TNF-α . Inhibition of FSH-dependent DNA synthesis by TNF-α was also found when cultures were co-stimulated with activin A. The inhibitory action of TN

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Short, Sarah M., Gregory A. Talbott, and Rudolph L. Juliano. "Integrin-mediated Signaling Events in Human Endothelial Cells." Molecular Biology of the Cell 9, no. 8 (August 1998): 1969–80. http://dx.doi.org/10.1091/mbc.9.8.1969.

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Vascular endothelial cells are important in a variety of physiological and pathophysiological processes. The growth and functions of vascular endothelial cells are regulated both by soluble mitogenic and differentiation factors and by interactions with the extracellular matrix; however, relatively little is known about the role of the matrix. In the present study, we investigate whether integrin-mediated anchorage to a substratum coated with the extracellular matrix protein fibronectin regulates growth factor signaling events in human endothelial cells. We show that cell adhesion to fibronecti

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Mattijssen, Sandy, and Richard J. Maraia. "LARP4 Is Regulated by Tumor Necrosis Factor Alpha in a Tristetraprolin-Dependent Manner." Molecular and Cellular Biology 36, no. 4 (December 7, 2015): 574–84. http://dx.doi.org/10.1128/mcb.00804-15.

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LARP4 is a protein with unknown function that independently binds to poly(A) RNA, RACK1, and the poly(A)-binding protein (PABPC1). Here, we report on its regulation. We found a conserved AU-rich element (ARE) in the human LARP4 mRNA 3′ untranslated region (UTR). This ARE, but not its antisense version or a point-mutated version, significantly decreased the stability of β-globin reporter mRNA. We found that overexpression of tristetraprolin (TTP), but not its RNA binding mutant or the other ARE-binding proteins tested, decreased cellular LARP4 levels. RNA coimmunoprecipitation showed that TTP s

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Izvolskaia, Marina, Viktoria Sharova, and Liudmila Zakharova. "Prenatal Programming of Neuroendocrine System Development by Lipopolysaccharide: Long-Term Effects." International Journal of Molecular Sciences 19, no. 11 (November 21, 2018): 3695. http://dx.doi.org/10.3390/ijms19113695.

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Various stress factors during critical periods of fetal development modulate the epigenetic mechanisms controlling specific genes, which can affect the structure and function of physiological systems. Maternal immune stress by bacterial infection simulated by lipopolysaccharide (LPS) in an experiment is considered to be a powerful programming factor of fetal development. Studies of the molecular mechanisms controlling the formation and functioning of physiological systems are in the pilot stage. LPSs are the most potent natural inflammation factors. LPS-induced increases in fetal levels of pro

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Mikhaylova, Irina V., Tiina Kuulasmaa, Jarmo Jääskeläinen та Raimo Voutilainen. "Tumor Necrosis Factor-α Regulates Steroidogenesis, Apoptosis, and Cell Viability in the Human Adrenocortical Cell Line NCI-H295R". Endocrinology 148, № 1 (1 січня 2007): 386–92. http://dx.doi.org/10.1210/en.2006-0726.

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TNF-α regulates the hypothalamo-pituitary-adrenal axis at several levels. It has been shown to modify adrenal steroidogenesis in many species, and it is supposed to act as an auto/paracrine factor. However, its significance in human adrenocortical function remains unclear. Therefore, we investigated the effect of TNF-α on adrenal steroidogenesis, expression of the key steroidogenic genes, apoptosis, and cell viability in the human adrenocortical cell line NCI-H295R. TNF-α treatment (1 nm for 48 h) decreased the basal production of cortisol, androstenedione, dehydroepiandrosterone sulfate (DHEA

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Tannenbaum, C. S., J. A. Major, and T. A. Hamilton. "IFN-gamma and lipopolysaccharide differentially modulate expression of tumor necrosis factor receptor mRNA in murine peritoneal macrophages." Journal of Immunology 151, no. 12 (December 15, 1993): 6833–39. http://dx.doi.org/10.4049/jimmunol.151.12.6833.

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Abstract Expression of TNF receptor (TNFR) mRNA has been examined in murine peritoneal macrophages stimulated with LPS and/or IFN-gamma. LPS markedly enhanced expression of a heterogenous population of mRNA, which hybridized with a cDNA encoding the type II TNFR. mRNA expression was optimally induced by 4 to 8 h and returned to baseline by 24 h after stimulation. Interestingly, though IFN-gamma can synergize with LPS for the expression of TNF-alpha, it abrogated the LPS-mediated enhancement of type II TNFR in a dose-dependent fashion. IFN-alpha, though less effective, had a qualitatively compa

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Halim, Sobia Ahsan, Almas Gul Sikandari, Ajmal Khan, Abdul Wadood, Muhammad Qaiser Fatmi, René Csuk та Ahmed Al-Harrasi. "Structure-Based Virtual Screening of Tumor Necrosis Factor-α Inhibitors by Cheminformatics Approaches and Bio-Molecular Simulation". Biomolecules 11, № 2 (22 лютого 2021): 329. http://dx.doi.org/10.3390/biom11020329.

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Tumor necrosis factor-α (TNF-α) is a drug target in rheumatoid arthritis and several other auto-immune disorders. TNF-α binds with TNF receptors (TNFR), located on the surface of several immunological cells to exert its effect. Hence, the use of inhibitors that can hinder the complex formation of TNF-α/TNFR can be of medicinal significance. In this study, multiple chem-informatics approaches, including descriptor-based screening, 2D-similarity searching, and pharmacophore modelling were applied to screen new TNF-α inhibitors. Subsequently, multiple-docking protocols were used, and four-fold po

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KUMAR, SUNIL, DOLKER LAMO, GEETA GAHLAWAT, VIJAY K. BHARTI, and KRISHNA KUMAR. "Effect of endurance load exercise on physio-biochemical and hormonal parameters of single-humped camels (Camelus dromedarius) at high altitude." Indian Journal of Animal Sciences 92, no. 7 (June 19, 2022): 837–42. http://dx.doi.org/10.56093/ijans.v92i7.115253.

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The present study was carried out for 7 days on four adult low-lander single-humped camels to know the effectof endurance load exercise on physiological, biochemical, hormonal, and inflammatory cytokines at high altitude.A significant 1.5 to 3 fold increase was observed in physiological responses, viz. the respiration and heart rate onthe 1st and 7th day after the load endurance exercise. Further, serum triglycerides levels were significantly increased on the 7th day after the load endurance exercise, whereas other biochemical parameters were unaffected. However, hormones and inflammatory cyto

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Denzler, Karen, Jessica Moore, Heather Harrington, Kira Morrill, Trung Huynh, Bertram Jacobs, Robert Waters, and Jeffrey Langland. "Characterization of the Physiological Response followingIn VivoAdministration ofAstragalus membranaceus." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/6861078.

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The botanical,Astragalus membranaceus, is a therapeutic in traditional Chinese medicine. Limited literature exists on the overallin vivoeffects ofA. membranaceuson the human body. This study evaluates the physiological responses toA. membranaceusby measuring leukocyte, platelet, and cytokine responses as well as body temperature and blood pressure in healthy individuals after thein vivoadministration ofA. membranaceus. A dose-dependent increase in monocytes, neutrophils, and lymphocytes was measured 8–12 hours after administration and an increase in the number of circulating platelets was seen

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Gao, Jing, Dongsheng Wang, Dan Liu, Min Liu, Yehua Ge, Minghong Jiang, Yanxin Liu, and Dexian Zheng. "Tumor necrosis factor–related apoptosis-inducing ligand induces the expression of proinflammatory cytokines in macrophages and re-educates tumor-associated macrophages to an antitumor phenotype." Molecular Biology of the Cell 26, no. 18 (September 15, 2015): 3178–89. http://dx.doi.org/10.1091/mbc.e15-04-0209.

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Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) is a promising candidate for cancer therapy, because it can induce apoptosis in various tumor cells but not in most normal cells. Although it is well known that TRAIL and its receptors are expressed in many types of normal cells, including immune cells, their immunological effects and regulatory mechanisms are still obscure. In the present study, we demonstrated that TRAIL affected the activity of NF-κB (nuclear factor-κB) and the expression of its downstream proinflammatory cytokines IL-1β (interleukin-1β), IL-6, and tumor necros

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Abe, Shogo, Misako Ueno, Mami Nishitani, Tetsuya Akamatsu, Takumi Sato, Marie Shimoda, Hiroki Kanaoka, Yoshitaka Nii, Hiroko Yamasaki, and Keizo Yuasa. "Citrus sudachi Peel Extract Suppresses Cell Proliferation and Promotes the Differentiation of Keratinocytes through Inhibition of the EGFR–ERK Signaling Pathway." Biomolecules 10, no. 10 (October 21, 2020): 1468. http://dx.doi.org/10.3390/biom10101468.

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Citrus sudachi is a well-known fruit in Tokushima Prefecture, Japan, and its peels are rich in phytochemicals, including phenolic compounds. Although it is expected that the extract of the C. sudachi peel elicits various beneficial physiological activities, the effect on the skin has not been investigated. In this study, we report that the aqueous extract from the peel of C. sudachi suppresses cell proliferation of the immortalized human keratinocyte cell line, HaCaT, and primary normal human epidermal keratinocytes. The extract of C. sudachi peel suppressed epidermal growth factor (EGF)-induc

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Mygind, Leda, Marianne Skov-Skov Bergh, Vivien Tejsi, Ramanan Vaitheeswaran, Kate L. Lambertsen, Bente Finsen, and Athanasios Metaxas. "Tumor Necrosis Factor (TNF) Is Required for Spatial Learning and Memory in Male Mice under Physiological, but Not Immune-Challenged Conditions." Cells 10, no. 3 (March 9, 2021): 608. http://dx.doi.org/10.3390/cells10030608.

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Increasing evidence demonstrates that inflammatory cytokines—such as tumor necrosis factor (TNF)—are produced at low levels in the brain under physiological conditions and may be crucial for synaptic plasticity, neurogenesis, learning and memory. Here, we examined the effects of developmental TNF deletion on spatial learning and memory using 11–13-month-old TNF knockout (KO) and C57BL6/J wild-type (WT) mice. The animals were tested in the Barnes maze (BM) arena under baseline conditions and 48 h following an injection of the endotoxin lipopolysaccharide (LPS), which was administered at a dose

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Mitlianga, P., G. Germanidis, H. M. Moutsopoulos та G. K. Papadopoulos. "The Effect of Transforming Growth Factor β1, and Tumor Necrosis Factor α on the Cytotoxic-Cytostatic Action of Interleukin-1 (α and β Isoforms) on the Pancreatic B Cell Line Rin-5ah". International Journal of Immunopathology and Pharmacology 8, № 2 (травень 1995): 67–77. http://dx.doi.org/10.1177/039463209500800201.

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The rat pancreatic β cell line RIN-5AH was treated with the cytokines IL-1 (α and β), TNFα and TGF-β1, in order to examine at the clonal level the reported mostly cytotoxic effects of IL-1, on isolated islets of Langerhans and islet cell preparations. In contrast to what has been previously reported for whole islets and islet cell preparations we find that IL-1 (α or β) is not cytotoxic to the RIN-5AH cells in logarithmic growth phase to any extent, even at very high cytokine concentrations (125 nM). Furthermore, TNFα does not in any way potentiate IL-1 cytotoxicity. Transforming growth factor

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Velayudhan, Silpa Mullakkalparambil, Kerstin Brügemann, Shahin Alam, Tong Yin, Chinnasamy Devaraj, Veerasamy Sejian, Eva Schlecht, and Sven König. "Molecular, Physiological and Hematological Responses of Crossbred Dairy Cattle in a Tropical Savanna Climate." Biology 12, no. 1 (December 23, 2022): 26. http://dx.doi.org/10.3390/biology12010026.

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A comprehensive study was conducted to assess the effects of seasonal transition and temperature humidity index (THI) on the adaptive responses in crossbred dairy cows reared in a tropical savanna region. A total of 40 lactating dairy cattle reared by small-scale dairy farmers in Bengaluru, India, were selected for this study. The research period comprised the transitioning season of summer to monsoon, wherein all traits were recorded at two points, one representing late summer (June) and the other early monsoon (July). A set of extensive variables representing physiological responses (pulse r

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Hill, Molly R., Stephen Clarke, Kerry Rodgers, Brandi Thornhill, Jeffrey M. Peters, Frank J. Gonzalez, and Jeffrey M. Gimble. "Effect of Peroxisome Proliferator-Activated Receptor Alpha Activators on Tumor Necrosis Factor Expression in Mice during Endotoxemia." Infection and Immunity 67, no. 7 (July 1, 1999): 3488–93. http://dx.doi.org/10.1128/iai.67.7.3488-3493.1999.

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ABSTRACT Inflammatory mediators orchestrate the host immune and metabolic response to acute bacterial infections and mediate the events leading to septic shock. Tumor necrosis factor (TNF) has long been identified as one of the proximal mediators of endotoxin action. Recent studies have implicated peroxisome proliferator-activated receptor alpha (PPARα) as a potential target to modulate regulation of the immune response. Since PPARα activators, which are hypolipidemic drugs, are being prescribed for a significant population of older patients, it is important to determine the impact of these dr

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Thomson, B. M., G. R. Mundy, and T. J. Chambers. "Tumor necrosis factors alpha and beta induce osteoblastic cells to stimulate osteoclastic bone resorption." Journal of Immunology 138, no. 3 (February 1, 1987): 775–79. http://dx.doi.org/10.4049/jimmunol.138.3.775.

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Abstract Antigen- or mitogen-stimulated leukocytes release bone-resorbing activity into culture supernatants in vitro. Among the agents likely to be present in such supernatants are monocyte-derived tumor necrosis factor (TNF-alpha) and lymphocyte-derived tumor necrosis factor (TNF-beta) (lymphotoxin), both of which have recently been shown to stimulate bone resorption in organ culture. To identify the mechanism of action of these agents, we compared bone resorption by isolated osteoclasts with bone resorption by osteoclasts cocultured with osteoblastic cells, and with bone resorption by osteo

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Chen, Yi-Jian, Li-Qun Zhang, Guang-Ping Wang, Hui Zeng, Ben Lü, Xu-Liang Shen, Zhi-Ping Jiang, and Fang-Ping Chen. "Adiponectin inhibits tissue factor expression and enhances tissue factor pathway inhibitor expression in human endothelial cells." Thrombosis and Haemostasis 100, no. 08 (2008): 291–300. http://dx.doi.org/10.1160/th08-02-0124.

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SummaryTissue factor (TF) plays a pivotal role in thrombus formation and atherogenesis in acute coronary syndrome. Tissue factor pathway inhibitor (TFPI) is a specific physiological inhibitor of TF/ FVIIa complex that regulates TF-induced coagulation. Adiponectin (Adp) is an adipocyte-specific adipocytokine with anti-atherogenic and anti-diabetic properties. Adp inhibits inflammatory cytokine and adhesion molecules expression, and it can prevent endothelial dysfunction. In this study, we investigated the effects of Adp on tumor necrosis factor-α (TNF-α)-induced expression of TF and TFPI in hum

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Bauldry, S. A., C. E. McCall, S. L. Cousart, and D. A. Bass. "Tumor necrosis factor-alpha priming of phospholipase A2 activation in human neutrophils. An alternative mechanism of priming." Journal of Immunology 146, no. 4 (February 15, 1991): 1277–85. http://dx.doi.org/10.4049/jimmunol.146.4.1277.

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Abstract The cytokine, TNF-alpha, interacts with human neutrophils (PMN) via specific membrane receptors and primes leukotriene B4 (LTB4) production in PMN for subsequent stimulation by calcium ionophores. We have further examined the effects of TNF-alpha on arachidonic acid (AA) release, LTB4 production, and platelet-activating factor (PAF) formation in PMN by prelabeling cells with either [3H]AA or [3H]lyso-PAF, priming with human rTNF-alpha, and then stimulating with the chemotactic peptide, FMLP. TNF-alpha, alone, had little effect; minimal AA release, LTB4 or PAF production occurred after

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Delfraissy, J. F., C. Wallon, F. Boue, F. Barresinoussi, and P. Galanaud. "Tumor necrosis factor-alpha inhibits the competence signal delivered by HIV to normal B cells." Journal of Immunology 146, no. 5 (March 1, 1991): 1516–21. http://dx.doi.org/10.4049/jimmunol.146.5.1516.

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Abstract Polyclonal B cell activation is commonly observed in HIV-infected patients. The coordinate delivery of a number of signals is required for B cell response. This work was designed to better define the role of HIV in the first steps of normal human B cells activation. We show that the infectious virus or recombinant envelope proteins can render B cells responsive to the growth-promoting effect of several T cell-derived IL, IL-2, IL-4, and low m.w. (12-kDa) BCGF. HIV acts in the absence of monocytes and on different populations of B cells. The competence signal can be provided by recombi

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Chung, Yi, Yi-Ting Hsiao, and Wen-Ching Huang. "Physiological and Psychological Effects of Treadmill Overtraining Implementation." Biology 10, no. 6 (June 10, 2021): 515. http://dx.doi.org/10.3390/biology10060515.

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Overtraining in athletes usually causes profound and lasting deleterious effects on the maintenance of health and exercise capacity. Here, we established an overtraining animal model to investigate the physiological modulation for future strategic applications in vivo. We subjected C57BL/6 mice to exhaustive treadmill exercises daily for 8 weeks (the exhaustive exercise group). Next, the physiological and psychological outcomes were compared with the regular exercise and sedentary groups. Outcome measures included growth, glucose tolerance, exercise metabolism profiles, cytokine levels, intest

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