scholarly journals Critical role of tumor necrosis factor receptor 1, but not 2, in hepatic stellate cell proliferation, extracellular matrix remodeling, and liver fibrogenesis

Hepatology ◽  
2011 ◽  
Vol 54 (1) ◽  
pp. 319-327 ◽  
Author(s):  
Núria Tarrats ◽  
Anna Moles ◽  
Albert Morales ◽  
Carmen García-Ruiz ◽  
José C. Fernández-Checa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Necrosis ◽  
Stellate Cell ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Liver Fibrogenesis ◽  
Necrosis Factor

scholarly journals Critical role of tumor necrosis factor receptor 1 in the pathogenesis of pulmonary emphysema in mice

2016 ◽  
Vol Volume 11 ◽  
pp. 1705-1712 ◽  
Author(s):  
Masaki Fujita ◽  
Ouchi Hiroshi ◽  
Satoshi Ikemage ◽  
Eiji Harada ◽  
Takemasa Matsumoto ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Pulmonary Emphysema ◽  
Tumor Necrosis ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor

scholarly journals TNFRSF14 deficiency protects against ovariectomy-induced adipose tissue inflammation

2014 ◽  
Vol 220 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Eun-Kyung Choi ◽  
Woon-Ki Kim ◽  
Ok-Joo Sul ◽  
Yun-Kyung Park ◽  
Eun-Sook Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
Tumor Necrosis ◽  
Ovarian Function ◽  
Tumor Necrosis Factor Receptor ◽  
Oxygen Species ◽  
Adipose Tissue Inflammation ◽  
Metabolic Perturbation ◽  
Necrosis Factor

To elucidate the role of tumor necrosis factor receptor superfamily member 14 (TNFRSF14) in metabolic disturbance due to loss of ovarian function, ovariectomy (OVX) was performed in TNFRSF 14-knockout mice. OVX increased fat mass and infiltration of highly inflammatory CD11c cells in the adipose tissue (AT), which was analyzed by flow cytometry, and resulted in disturbance of glucose metabolism, whereas TNFRSF14 deficiency attenuated these effects. TNFRSF14 deficiency decreased recruitment of CD11c-expressing cells in AT and reduced the polarization of bone marrow-derived macrophages to M1. Upon engagement of LIGHT, a TNFRSF14 ligand, TNFRSF14 enhanced the expression of CD11c via generation of reactive oxygen species, suggesting a role of TNFRSF14 as a redox modulator. TNFRSF14 participated in OVX-induced AT inflammation via upregulation of CD11c, resulting in metabolic perturbation. TNFRSF14 could be used as a therapeutic target for the treatment of postmenopausal syndrome by reducing AT inflammation.

The Role of the Tumor Necrosis Factor Receptor in 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-Induced Colitis in Mice

2005 ◽  
Vol 50 (9) ◽  
pp. 1669-1676 ◽  
Author(s):  
Minoru Nakai ◽  
Kaori Sudo ◽  
Yasuhiro Yamada ◽  
Yasushi Kojima ◽  
Tomohiro Kato ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Sulfonic Acid ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Trinitrobenzene Sulfonic Acid ◽  
Necrosis Factor

scholarly journals Opposing role of tumor necrosis factor receptor 1 signaling in T cell-mediated hepatitis and bacterial infection in mice

Hepatology ◽  
2016 ◽  
Vol 64 (2) ◽  
pp. 508-521 ◽  
Author(s):  
Raluca Wroblewski ◽  
Marietta Armaka ◽  
Vangelis Kondylis ◽  
Manolis Pasparakis ◽  
Henning Walczak ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Necrosis Factor ◽  
Bacterial Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor

MO071PROTEINS LINKED TO ATHEROSCLEROSIS AND CELL PROLIFERATION ARE ASSOCIATED WITH SHRUNKEN PORE SYNDROME IN HEART FAILURE PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Liana Xhakollari ◽  
Amra Jujic ◽  
John Molvin ◽  
Peter M Nilsson ◽  
Hannes Holm ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Proliferation ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Scavenger Receptor ◽  
Interleukin 2 ◽  
Tumor Necrosis Factor Receptor ◽  
Heart Failure Patients ◽  
Cardiovascular Morbidity And Mortality ◽  
Necrosis Factor

Abstract Background and Aims The “Shrunken pore syndrome” is characterized by a difference in renal filtration between cystatin C and creatinine resulting in a low eGFRcystatinC/eGFRcreatinine-ratio, and studies have demonstrated a high risk for cardiovascular morbidity and mortality for patients with shrunken pore syndrome. In this observational study, we explored associations between shrunken pore syndrome and proteins implicated in cardiovascular disease and inflammation in patients with heart failure. Method Plasma samples from 300 individuals HARVEST-Malmö trial hospitalized for the diagnosis of heart failure (mean age 75 years; 30% female), were analyzed with a proximity extension assay consisting of 92 proteins, to identify proteins associated with shrunken pore syndrome. Shrunken pore syndrome was defined as eGFRcystatinC ≤60% of eGFRcreatinine. Proteins associated with shrunken pore syndrome in the initial age and sex-adjusted analyses (Bonferroni-corrected p≤ 5.4x10-4) were further adjusted for relevant covariates. Results In multivariate analyses, Shrunken pore syndrome was associated with elevated levels of six proteins; scavenger receptor cysteine-rich type 1 protein M130, tumor necrosis factor receptor 1, tumor necrosis factor receptor 2, osteoprotegerin, interleukin-2 receptor subunit alpha, and tyrosine-protein kinase receptor UFO (p<0.05). Conclusion In heart failure patients, shrunken pore syndrome was independently associated with proteins linked to atherosclerosis and cell proliferation.

Tumor Necrosis Factor Receptor-Associated Factor 5 Promotes Arterial Neointima Formation through Smooth Muscle Cell Proliferation

2019 ◽  
Vol 56 (6) ◽  
pp. 308-319
Author(s):  
Florian Willecke ◽  
Benjamin Rupprecht ◽  
Mark Colin Gissler ◽  
Katharina Pfeiffer ◽  
Nathaly Anto-Michel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Smooth Muscle Cell Proliferation ◽  
Neointima Formation ◽  
Necrosis Factor

scholarly journals A Critical Role of the p75 Tumor Necrosis Factor Receptor (p75TNF-R) in Organ Inflammation Independent of  TNF, Lymphotoxin α, or the p55TNF-R

1998 ◽  
Vol 188 (7) ◽  
pp. 1343-1352 ◽  
Author(s):  
Eleni Douni ◽  
George Kollias
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Peripheral Blood Mononuclear ◽  
Enhanced Production ◽  
Wide Range ◽  
Lymphotoxin Α ◽  
Necrosis Factor

Despite overwhelming evidence that enhanced production of the p75 tumor necrosis factor receptor (p75TNF-R) accompanies development of specific human inflammatory pathologies such as multi-organ failure during sepsis, inflammatory liver disease, pancreatitis, respiratory distress syndrome, or AIDS, the function of this receptor remains poorly defined in vivo. We show here that at levels relevant to human disease, production of the human p75TNF-R in transgenic mice results in a severe inflammatory syndrome involving mainly the pancreas, liver, kidney, and lung, and characterized by constitutively increased NF-κB activity in the peripheral blood mononuclear cell compartment. This process is shown to evolve independently of the presence of TNF, lymphotoxin α, or the p55TNF-R, although coexpression of a human TNF transgene accelerated pathology. These results establish an independent role for enhanced p75TNF-R production in the pathogenesis of inflammatory disease and implicate the direct involvement of this receptor in a wide range of human inflammatory pathologies.

Sign in / Sign up

Export Citation Format

Share Document