Relevant bibliographies by topics / Tumor necrosis factor – Receptors – Physiological effect

Academic literature on the topic 'Tumor necrosis factor – Receptors – Physiological effect'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Tumor necrosis factor – Receptors – Physiological effect"

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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 (∼38 ml/kg) for 2 h or until they developed arterial hypotension. Pulmonary edema was assessed by physiological parameters including respiratory mechanics and blood gases, and by lavage fluid protein, lung wet:dry weight ratio, and lung permeability measurements using fluorescence-labeled albumin. High stretch ventilation in wild-type and TNF receptor double knockout animals induced similar pulmonary edema, and only 25–30% of mice completed the protocol. In contrast, the p55 receptor knockout mice were strongly protected from edema formation, with all animals completing the protocol. Myeloperoxidase assay indicated that this protective effect was not associated with decreased pulmonary neutrophil sequestration. The p75 receptor knockout mice, however, displayed increased susceptibility to edema formation, and no animals survived the full 2 h. These results demonstrate a novel role for TNF signaling (independent from its effects on neutrophil recruitment) specifically through the p55 receptor, in promoting high stretch-induced pulmonary edema, whereas p75 signaling may play an opposing role.
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2

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-NMMA; 300 microM). TNF-alpha (0.00417, 0.0417, 0.417, and 1.25 micrograms/ml) incubated with BPA for 60 min inhibited EDR of the BPA to ACh, BK, and histamine. The effects of TNF required 30 min for onset. Recovery of EDR occurred 3–4 h after washout of TNF-alpha. Pentoxifylline (1 microM) did not affect ACh-induced EDR but selectively reversed TNF-alpha-mediated inhibition of ACh-induced EDR. TNF-alpha-mediated inhibition of EDR was not reversible by L-NMMA, an inhibitor of NOS I and NOS II, the cyclooxygenase inhibitor ibuprofen, or CV-3908 (1 microM), a platelet-activating factor antagonist. The inhibitory effect of TNF-alpha on EDR was not mediated by nonspecific sensitization of the endothelium to human protein because recombinant human granulocyte colony-stimulating factor (10, 50, and 500 x 10(3) U/ml) did not affect EDR of BPA. The effect of TNF-alpha was specific for release of NO from the endothelium of BPA because TNF-alpha did not affect 1) EDR of BPV to ACh, BK, or ATP; 2) EIR of BPA or BPV to nitroprusside; and 3) contraction of either BPA or BPV to KCl, U-46619, histamine, norepinephrine, or serotonin. Thus TNF-alpha appears to selectively inhibit receptor-mediated EDR and NO release in BPA. TNF-alpha-mediated inhibition of EDR differs from that of L-arginine-based inhibitors and may represent an endogenous physiological mechanism of regulation of NO in the endothelium.
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Schuld, A., J. Mullington, D. Hermann, D. Hinze-Selch, T. Fenzel, F. Holsboer, and T. Pollmächer. "Effects of granulocyte colony-stimulating factor on night sleep in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 4 (April 1, 1999): R1149—R1155. http://dx.doi.org/10.1152/ajpregu.1999.276.4.r1149.

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Numerous animal studies suggest that cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) mediate increased sleep amount and intensity observed during infection and are, moreover, involved in physiological sleep regulation. In humans the role of cytokines in sleep-wake regulation is largely unknown. In a single-blind, placebo-controlled study, we investigated the effects of granulocyte colony-stimulating factor (G-CSF, 300 μg sc) on the plasma levels of cytokines, soluble cytokine receptors, and hormones as well as on night sleep. G-CSF did not affect rectal temperature or the plasma levels of cortisol and growth hormone but did induce increases in the plasma levels of IL-1 receptor antagonist and both soluble TNF receptors within 2 h after injection. In parallel, the amount of slow-wave sleep and electroencephalographic delta power were reduced, indicating a lowered sleep intensity. We conclude that G-CSF suppresses sleep intensity via increased circulating amounts of endogenous antagonists of IL-1β and TNF-α activity, suggesting that these cytokines are involved in human sleep regulation.
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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 these SAPKs is associated with the effects of 1,25(OH)(2)D(3) on keratinocytes under stress. HaCaT keratinocytes were exposed to heat shock, hyperosmotic concentrations of sorbitol, the epidermal growth factor receptor tyrosine kinase inhibitor AG1487, the pro-inflammatory cytokine tumor necrosis factor alpha, and H(2)O(2). These stresses activated both SAPKs. Pretreatment with 1,25(OH)(2)D(3) inhibited the activation of JNK by all stresses and the activation of p38 by heat shock, AG1478 and tumor necrosis factor alpha. Under the same conditions, treatment with 1,25(OH)(2)D(3) protected HaCaT keratinocytes from cytotoxicity induced by exposure to H(2)O(2) and hyperosmotic shock. The effect of 1,25(OH)(2)D(3) was dose-dependent, already apparent at nanomolar concentrations, and time-dependent, maximal after a 24-h pre-incubation. We suggest that inhibition of SAPK activation may account for some of the well-documented protective effects of 1,25(OH)(2)D(3) on epidermal cells during exposure to UV or chemotherapy and may also be related to the anti-inflammatory actions of the hormone in skin.
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Mamińska, Agnieszka, Anna Bartosik, Magdalena Banach-Orłowska, Iwona Pilecka, Kamil Jastrzębski, Daria Zdżalik-Bielecka, Irinka Castanon, et al. "ESCRT proteins restrict constitutive NF-κB signaling by trafficking cytokine receptors." Science Signaling 9, no. 411 (January 19, 2016): ra8. http://dx.doi.org/10.1126/scisignal.aad0848.

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Because signaling mediated by the transcription factor nuclear factor κB (NF-κB) is initiated by ligands and receptors that can undergo internalization, we investigated how endocytic trafficking regulated this key physiological pathway. We depleted all of the ESCRT (endosomal sorting complexes required for transport) subunits, which mediate receptor trafficking and degradation, and found that the components Tsg101, Vps28, UBAP1, and CHMP4B were essential to restrict constitutive NF-κB signaling in human embryonic kidney 293 cells. In the absence of exogenous cytokines, depletion of these proteins led to the activation of both canonical and noncanonical NF-κB signaling, as well as the induction of NF-κB–dependent transcriptional responses in cultured human cells, zebrafish embryos, and fat bodies in flies. These effects depended on cytokine receptors, such as the lymphotoxin β receptor (LTβR) and tumor necrosis factor receptor 1 (TNFR1). Upon depletion of ESCRT subunits, both receptors became concentrated on and signaled from endosomes. Endosomal accumulation of LTβR induced its ligand-independent oligomerization and signaling through the adaptors TNFR-associated factor 2 (TRAF2) and TRAF3. These data suggest that ESCRTs constitutively control the distribution of cytokine receptors in their ligand-free state to restrict their signaling, which may represent a general mechanism to prevent spurious activation of NF-κB.
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6

Pamir, Nathalie, Timothy S. McMillen, Karl J. Kaiyala, Michael W. Schwartz, and Renée C. LeBoeuf. "Receptors for Tumor Necrosis Factor-α Play a Protective Role against Obesity and Alter Adipose Tissue Macrophage Status." Endocrinology 150, no. 9 (May 28, 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 evaluated by quantifying plasma adipokine levels and macrophage-specific gene expression in fat. RKO mice were heavier (10%) and fatter (18%) than WT controls at 4 wk of age and were 26% heavier and 50% fatter than WT after 14 wk of HFHS diet feeding. Age- and diet-adjusted 24-h oxygen consumption, activity, and respiratory exchange ratio were significantly reduced in RKO mice. Obese RKO mice were markedly insulin resistant, suggesting that intact TNFR signaling is not required for the effect of obesity to impair glucose metabolism. Adipose tissue from HFHS-fed RKO mice exhibited increased macrophage infiltration, but compared with WT mice, macrophage phenotypic markers featured a predominance of antiinflammatory M2 over proinflammatory M1 cells. TNFRs play a physiological role to limit body weight and adiposity by modestly increasing metabolic rate and fatty acid oxidation, and they are required for obesity-induced activation of adipose tissue macrophages. Despite these effects, TNFRs are not required for obesity-induced insulin resistance.
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Caldwell, J., and SG Emerson. "Interleukin-1 alpha upregulates tumor necrosis factor receptors expressed by a human bone marrow stromal cell strain: implications for cytokine redundancy and synergy." Blood 86, no. 9 (November 1, 1995): 3364–72. http://dx.doi.org/10.1182/blood.v86.9.3364.bloodjournal8693364.

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To explore the biochemical and physiologic basis of the overlapping effects of interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor alpha (TNF-alpha) on myeloid cytokine production, we have studied the dynamics of granulocyte colony-stimulating factor (G-CSF) and granulocyte-monocyte colony-stimulating factor (GM-CSF) production as well as IL-1 receptor and TNF receptor expression in a clonally derived bone marrow stromal cell strain (CDCL). IL-1 alpha and TNF alpha act in a synergistic manner to stimulate G-CSF and GM-CSF production by CDCL, resulting in an increase in CSF secretion that is 250-fold greater than that observed with either cytokine alone. This synergism in protein secretion is paralleled by synergistic increases the steady-state level of GM- and G-CSF mRNA, with supra-additive levels achieved by 24 hours. Coincident with this synergistic induction of myeloid CSFs, treatment of CDCL cells with IL-1 alpha induces a 300% increase in the expression of TNF receptors. IL-1 alpha induction of TNF receptors reaches a peak after 6 hours and gradually returns to baseline level by 24 hours. IL-1 alpha does not affect TNF receptor ligand binding affinity. A kinetic study comparing IL-1/TNF synergistic induction of growth factor secretion with IL-1 alpha induction of TNF receptors shows that these events occur in parallel. In contrast with the induction of TNF receptors by IL-1 alpha, treatment with TNF alpha has no effect on either the number of IL-1 receptors expressed by CDCL cells or IL-1 receptor ligand binding affinity. Brief treatment of IL-1 alpha/TNF alpha-stimulated CDCL cells with cycloheximide before receptor induction reduces the synergistic increase in growth factor mRNA by 40% to 60% compared with cells not treated with CHX. Taken together, these results raise the possibility that IL-1 alpha cross-induction of TNF receptors may contribute to the biochemical mechanisms underlying the synergistic stimulation of G-CSF and GM-CSF production by IL-1 alpha and TNF alpha.
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8

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 fibronectin and growth factor stimulation trigger distinct initial tyrosine phosphorylation events in endothelial cells. Thus, integrin-dependent adhesion of endothelial cells leads to tyrosine phosphorylation of both focal adhesion kinase and paxillin, but not of several growth factor receptors. Conversely, EGF stimulation causes receptor autophosphorylation, with no effect on focal adhesion kinase or paxillin tyrosine phosphorylation. Adhesion to fibronectin, in the absence of growth factors, leads to activation of MAPK. In addition, adhesion to fibronectin also potentiates growth factor signaling to MAPK. Thus, polypeptide growth factor activation of MAPK in anchored cells is far more effective than in cells maintained in suspension. Other agonists known to activate MAPK were also examined for their ability to activate MAPK in an anchorage-dependent manner. The neuropeptide bombesin, the bioactive lipid lysophosphatidic acid (LPA), and the cytokine tumor necrosis factor α, which signal through diverse mechanisms, were all able to activate MAPK to a much greater degree in fibronectin-adherent cells than in suspended cells. In addition, tumor necrosis factor α activation of c-Jun kinase (JNK) was also much more robust in anchored cells. Together, these data suggest a cooperation between integrins and soluble mitogens in efficient propagation of signals to downstream kinases. This cooperation may contribute to anchorage dependence of mitogenic cell cycle progression.
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9

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 comparable effect. These effects were selective for the type II TNFR because levels of mRNA encoding the type I TNFR did not vary appreciably with any of the treatments described. The effects of IFN-gamma on LPS-mediated TNFR expression were dependent on the sequence of exposure; pretreatment with IFN-gamma was most effective at blocking response to LPS, whereas IFN-gamma added 1 h after initiation of LPS treatment had little or no effect. The effects of both LPS and IFN-gamma on type II TNFR expression were mediated at least in part by modulation of transcription. The effects of both LPS and IFN-gamma were also independent of protein synthesis because inclusion of cycloheximide in the treatment protocol did not abrogate either the inductive or the suppressive effects. These findings suggest that IFN-gamma and LPS modulate the physiologic action of TNF through complex mechanisms involving effects on the transcription of TNF-alpha itself and on receptors through which it may act in autocrine or paracrine fashion.
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10

Guarnieri, Giulia, Erica Sarchielli, Paolo Comeglio, Erika Herrera-Puerta, Irene Piaceri, Benedetta Nacmias, Matteo Benelli, et al. "Tumor Necrosis Factor α Influences Phenotypic Plasticity and Promotes Epigenetic Changes in Human Basal Forebrain Cholinergic Neuroblasts." International Journal of Molecular Sciences 21, no. 17 (August 25, 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 increased the expression of TNFα receptor TNFR2 and the mature neuron marker MAP2, also promoting neurite elongation. Moreover, TNFα affected nerve growth factor receptor expression. We also found that TNFα induced the expression of DNA-methylation enzymes and, accordingly, downregulated genes involved in neuronal development through epigenetic mechanisms, as demonstrated by methylome analysis. In summary, TNFα showed a dual role on hfNBMs phenotypic plasticity, exerting a negative influence on neurogenesis despite a positive effect on differentiation, through mechanisms that remain to be elucidated. Our results help to clarify the complexity of TNFα effects in human neurons and suggest that manipulation of TNFα signaling could provide a potential therapeutic approach against neurodegenerative disorders.
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Dissertations / Theses on the topic "Tumor necrosis factor – Receptors – Physiological effect"

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Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.

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Caughey, Gillian Elizabeth. "Regulation of interleukin-1[Beta] and tumor necrosis factor[alpha] synthesis by fatty acids and eicosanoids /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phc371.pdf.

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Penglis, Peter Savas. "The relationships between eicosanoid production and pro-inflammatory cytokines." Title page, contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09php3985.pdf.

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Includes bibliographical references (leaves 182-240). Explores alternate strategies that may alter inflammatory cytokine production, particularly tumour necrosis factor đ [tumor necrosis factor-alpha], and therefore provide a possible treatment for rheumatoid arthritis.
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Barbara, Jeffrey A. J. (Jeffrey Allan J. ). "The mechanism of action of tumour necrosis factor-[alpha] / Jeffrey A.J. Barbara." 1995. http://hdl.handle.net/2440/18552.

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Amendments inserted inside front cover.
Bibliograpghy: leaves 111-139.
xvi, 139, [29] leaves, [10] leaves of plates : ill. ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
The in vivo adminstration of Tumour Necrosis Factor-alpha as an antineoplastic agent has been severely restricted by dose-limiting side effects. Human TNF mutants with selective binding to the Human TNF receptors were employed to examine the role of these receptors in the mediation of TNF's cytotoxic and proinflammatory activities.
Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1995?
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Barbara, Jeffrey A. J. (Jeffrey Allan J. ). "The mechanism of action of tumour necrosis factor-α / Jeffrey A.J. Barbara." Thesis, 1995. http://hdl.handle.net/2440/18552.

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Amendments inserted inside front cover.
Bibliograpghy: leaves 111-139.
xvi, 139, [29] leaves, [10] leaves of plates : ill. ; 30 cm.
The in vivo adminstration of Tumour Necrosis Factor-alpha as an antineoplastic agent has been severely restricted by dose-limiting side effects. Human TNF mutants with selective binding to the Human TNF receptors were employed to examine the role of these receptors in the mediation of TNF's cytotoxic and proinflammatory activities.
Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1995?
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Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha / by Yvelle Hope Atkinson." Thesis, 1989. http://hdl.handle.net/2440/18993.

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Ng, Esther Mei Ther. "The biological role of membrane tumour necrosis factor in inflammation and infection." Phd thesis, 2009. http://hdl.handle.net/1885/148364.

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Penglis, Peter Savas. "The relationships between eicosanoid production and pro-inflammatory cytokines." Thesis, 2001. http://hdl.handle.net/2440/111707.

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Explores alternate strategies that may alter inflammatory cytokine production, particularly tumour necrosis factor α [tumor necrosis factor-alpha], and therefore provide a possible treatment for rheumatoid arthritis.
Thesis (Ph.D.) -- University of Adelaide, Dept. of Medicine, 2001
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Gamble, Jennifer R. "Regulation of leukocyte adhesion to endothelium / by Jennifer Ruth Gamble." 1994. http://hdl.handle.net/2440/21552.

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Copies of author's previously published articles inserted.
Includes bibliographical references.
vii, 39 leaves : ill. ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Shows that the cytokine tumour necrosis factor [alpha] (TNF-[alpha]) enhances the adhesion of neutrophils to the endothelium by an action both on the neutrophil and on the endothelial cell.
Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1995?
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Gamble, Jennifer R. "Regulation of leukocyte adhesion to endothelium / by Jennifer Ruth Gamble." Thesis, 1994. http://hdl.handle.net/2440/21552.

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Copies of author's previously published articles inserted.
Includes bibliographical references.
vii, 39 leaves : ill. ; 30 cm.
Shows that the cytokine tumour necrosis factor [alpha] (TNF-[alpha]) enhances the adhesion of neutrophils to the endothelium by an action both on the neutrophil and on the endothelial cell.
Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1995?
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Books on the topic "Tumor necrosis factor – Receptors – Physiological effect"

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service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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Benjamin, Bonavida, ed. Tumor necrosis factor/cachectin and related cytokines. Basel: Karger, 1988.

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Marialuisa, Melli, and Parente Luca, eds. Cytokines and lipocortins in inflammation and differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of IL-1, TNF, and Lipocortins in Inflammation and Differentiation, held in Siena, Italy, October 22-25, 1989. New York, NY: Wiley-Liss, 1990.

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Kalthoff, Holger. Death Receptors and Cognate Ligands in Cancer. Springer, 2012.

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(Editor), Marialuisa Melli, and Luca Parente (Editor), eds. Cytokines and Lipocortins in Inflammation and Differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of Il-1, (Progress in Clinical & Biological Research). Wiley-Liss, 1990.

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Book chapters on the topic "Tumor necrosis factor – Receptors – Physiological effect"

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Longhi, L., F. Ortolano, E. R. Zanier, C. Perego, N. Stocchetti, and M. G. De Simoni. "Effect of traumatic brain injury on cognitive function in mice lacking p55 and p75 tumor necrosis factor receptors." In Acta Neurochirurgica Supplements, 409–13. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-85578-2_80.

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Hadem, Khetbadei Lysinia Hynniewta, Lakhon Kma, Rajeshwar N. Sharan, and Arnab Sen. "Anticancer Effect of Aristolochia tagala and Curcuma caesia Acting Through Tumor Necrosis Factor-a." In Handbook of Research on Advanced Phytochemicals and Plant-Based Drug Discovery, 366–94. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-5129-8.ch019.

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This chapter begins with a brief description of the events associated with carcinogenesis such as what led a normal cell to transform into a pre-neoplastic one, their multiplication, and development into cancer. The authors also described how reactive oxygen species (ROS) are generated endogenously and from carcinogens, their role in carcinogenesis, and the link between inflammation and cancer. Elucidation of how cancer arises contributes to understanding the molecular mechanisms of action of some natural products. Herbal natural products contain metabolites that exert a physiological action on human body. These metabolites are used therapeutically in modern medical practices to prevent and cure various diseases including cancer. This chapter discusses the anticancer property of two herbal plants Aristolochia tagala Cham. and Curcuma caesia Roxb. in diethylnitrosamine-induced mouse liver cancer and describes the most probable molecular mechanisms of action of the metabolites present in these plants contributing to their anticancer effect.
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Conference papers on the topic "Tumor necrosis factor – Receptors – Physiological effect"

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Loskutoff, D. J., J. Mimuro, and C. Hekman. "PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644763.

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Plasminogen activation provides an important source of localized proteolytic activity not only during fibrinolysis, but also during ovulation, cell migration, epithelial cell differentiation, tumor invasion and a variety of other physiological processes. Precise regulation of plasminogen activator (PA) activity thus constitutes a critical feature of many biological processes. This control is achieved in large part through the action of specific PA inhibitors (PAIs). Although 4 distinct PAIs have been detected,1the endothelial cellTderived inhibitor (PAI-1) is the only one that efficiently inhibits both urokinase (Kd=2.3×10−13M; Kassoc =1.6×108 M−1s−1) and single-chaintissue-type PA (tPA; Kd=1.3×lO−15 M Kd=3.9×lO7M−1s−1). It also inhibits trypsin (Kassoc=6.8×106M−1 s−1 ) ancl Plasmin (Kassoc=7.6×l05 M−1 s5 Analysis of the effect of PAI-1 on the rate of plasminogen activation revealed a competitive type of inhibition when urokinase was employed but a linear mixed type of inhibition when single chain tPA was employed. These results suggest that the interaction of PAI-1 with tPA, in contrast to its interaction with urokinase, may involve 2 sites on the tPA molecule.PAI-1 has been purified from medium conditioned by cultured bovine aortic endothelial cells and partially characterized. It is a major biosynthetic product of these cells, accounting for as much as 12% of the total protein released by the cells in 24 h. It has an M of 50,000, an isoelectric point of 4.5-5.0, and is immunologically and biochemically related to the rapidly acting inhibitor present in human platelets and in the plasma of some patients at risk to develop thrombotic problems. Although it is relatively stable to conditions which inactivate most protease inhibitors (acid pH, SDS), it is extremely sensitive to oxidants. The molecular cloning of the PAI-1 gene revealed that the mature human protein is 379 amino acids long, contains an NH2-terminal valine, lacks cysteines and has a methionine at the Pi position of it's reactive center. The conversion of this methionine to methionine sulfoxide may be responsible for the rapid inactivation of PAI-1 by oxidants. Human PAI-1 has extensive (30%) homology with α1-antitrypsin and antithrombin III and is thus a member of the serine proteinase inhibitor (serpin) family; a group of related molecules that control the major protease cascades of the blood. The PAI-1 gene is approximately 12.2 kilobase pairs in length and is organized into nine exons and eight introns.The production of PAI-1 by endothelial cells is stimulated by endotoxin, interleukin-1, tumor necrosis factor, and transforming growth factor β(TGFβ). The cells are extremely sensitive to TGFβwith maximal effects (100-fold stimulation) observed with 1-2 ng/ml. These changes were relatively specific for PAI-1, and could be detected at both the protein and the RNA level. Interestingly, TGFgalso stimulated the amount of PAI-1 present in the extracellular matrix (ECM) of BAEs. PAI-1 was one of the primary ECM components of these cells, constituting 10-20% of the ECM proteins detected after SDS-PAGE.One of the most unusual properties of PAI-1 is that it exists in blood and in various cellular samples in both an active and an inactive (latent) form, the ratio depending on the source. The latent form can be converted into the active one by treatment with denaturants like SDS or guanidine-HCl. Although the majority of the cell-associated PAI-1 is active, it rapidly decays (t1/2=3 h) into the latent form once it is released from the cells. In contrast, the half-life of ECM associated PAI-1 was greater than 24 h. These data suggest that PAI-1 is produced by BAEs in an active form, and is then either released into the medium where it is rapidly inactivated, or released into the subendothelium where it binds to ECM. The specific binding of PAI-1 to ECM protects it from this inactivation.
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Reports on the topic "Tumor necrosis factor – Receptors – Physiological effect"

1

Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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Abstract:
The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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