Polymorphism A36G of the tumor necrosis factor receptor 1 gene is associated with PAI-1 levels in obese women

2007 ◽  
Vol 97 (01) ◽  
pp. 62-66 ◽  
Author(s):  
Alenka Mavri ◽  
Delphine Bastelica ◽  
Marjorie Poggi ◽  
Pierre Morange ◽  
Franck Peiretti ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Plasma Concentrations ◽  
Tumor Necrosis Factor Receptor ◽  
Tnf Receptor ◽  
Obese Women ◽  
The Metabolic Syndrome ◽  
Necrosis Factor ◽  
Pai 1

SummaryThe tumor necrosis factor (TNF) pathway may be implicated in etiopathogenesis of PAI-1 overexpression during obesity. The aim of this study was to investigate the influence of polymorphismA36G of the TNF receptor 1 (TNFRSF1A +36A/G) on plasma concentrations of PAI-1 in 163 obese (31 with the metabolic syndrome, MetS) and 150 lean, healthy women. Genotypic and allele frequencies did not significantly differ between obese and lean subjects. TNFRSF1A genotypes were significantly associated with sTNFR1 plasma levels in obese women only (p<0.01); TNFRSF1A +36G/G obese carriers exhibited higher sTNFR1 and PAI-1 levels than A carriers (p<0.01 and p<0.05, respectively). In obese women, the presence of the MetS significantly potentiated the elevation of sTNFR1 and PAI-1 levels observed in the TNFRSF1A+36G/G carriers. Our results suggest that association between TNFRSF1A +36G/G genotype and the MetS renders obese women more prone to activation of the TNF pathway reflected by high circulating sTNFR1 and PAI-1 levels.

scholarly journals Emerging roles of C1Q tumor necrosis factor-related proteins in metabolic diseases

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Manjunath Ramanjaneya ◽  
Jayakumar Jerobin ◽  
Ilham Bettahi ◽  
Kodappully Sivaraman Siveen ◽  
Abdul-Badi Abou-Samra
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Metabolic Disorders ◽  
Pharmacological Intervention ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Related Proteins ◽  
Necrosis Factor

AbstractObesity and insulin resistance are key elements of the metabolic syndrome, which includes type 2 diabetes (T2D), dyslipidemia, systemic inflammation, hypertension, elevated risk for cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS). C1Q Tumor necrosis factor-related proteins (CTRPs) have recently emerged as important regulators of metabolism as a core component in the interrelationship between insulin resistance, adiposity and inflammation. To date 15 CTRP members have been identified and most of the CTRPs are dysregulated in obesity, T2D, coronary artery disease and NAFLD. Pharmacological intervention and lifestyle modification alter expression of CTRPs in circulation and in metabolically active tissues. CTRPs enhance metabolism mainly through activation of AMPK/AKT dependent pathways and possess insulin sensitizing properties. Thus dysregulated expression of CTRPs in metabolic disorders could contribute to the pathogenesis of the disease. For these reasons CTRPs appear to be promising targets for early detection, prevention and treatment of metabolic disorders. This review article aims at exploring the role of CTRPs in metabolic syndrome.

scholarly journals Maternal plasma concentrations of the soluble tumor necrosis factor receptor 2 are increased prior to the diagnosis of preeclampsia

2009 ◽  
Vol 200 (6) ◽  
pp. 630.e1-630.e8 ◽  
Author(s):  
Baha Sibai ◽  
Roberto Romero ◽  
Mark A. Klebanoff ◽  
Madeline Murguia Rice ◽  
Steve Caritis ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Plasma Concentrations ◽  
Tumor Necrosis Factor Receptor ◽  
Maternal Plasma ◽  
Necrosis Factor

Plasma concentrations of soluble tumor necrosis factor receptor I and tumor necrosis factor during cardiopulmonary bypass

2000 ◽  
Vol 70 (4) ◽  
pp. 1313-1318 ◽  
Author(s):  
Colleen W Marano ◽  
Leah Ann Garulacan ◽  
Kathleen V Laughlin ◽  
Lisa Igidbashian ◽  
Candace Trace ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Plasma Concentrations ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor

Tumor necrosis factor alpha gene G-308A polymorphism in the metabolic syndrome

Metabolism ◽  
2000 ◽  
Vol 49 (8) ◽  
pp. 1021-1024 ◽  
Author(s):  
Shao C. Lee ◽  
Yong Bing Pu ◽  
G.Neil Thomas ◽  
Zoe S.K. Lee ◽  
Brian Tomlinson ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
The Metabolic Syndrome ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

scholarly journals An Unusual Case of Allergic Reaction to Anakinra in a Patient with Tumor Necrosis Factor Receptor-1 Associated Periodic Syndrome (TRAPS) and Subsequent Canakinumab Treatment

2020 ◽  
Author(s):  
Marta Mejias Trueba ◽  
Marta Alonso Moreno ◽  
Noemi Garrido Puñal ◽  
Maria Soriano Martinez
Keyword(s):  
Tumor Necrosis Factor ◽  
Allergic Reaction ◽  
Tumor Necrosis ◽  
Unusual Case ◽  
Symptom Control ◽  
Tumor Necrosis Factor Receptor ◽  
Periodic Syndrome ◽  
Tnf Receptor ◽  
Biologic Drug ◽  
Necrosis Factor

Tumor necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS) is a rare hereditary systemic autoinflammatory disease (SAID). Treatment is based on corticosteroids, but often requires the addition of a biologic drug (anti-TNF agent, IL-1 receptor antagonist, etc) to achieve symptom control. The addition of the second drug is not clearly defined and must take into account the characteristics and preferences of the patient. We describe a patient with TRAPS and an allergic reaction to anakinra which was difficult to manage clinically while alternative treatment was being identified.

scholarly journals Suppression of Stroke-Induced Progenitor Proliferation in Adult Subventricular Zone by Tumor Necrosis Factor Receptor 1

2008 ◽  
Vol 28 (9) ◽  
pp. 1574-1587 ◽  
Author(s):  
Robert E Iosif ◽  
Henrik Ahlenius ◽  
Christine T Ekdahl ◽  
Vladimer Darsalia ◽  
Pär Thored ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Necrosis Factor ◽  
Subventricular Zone ◽  
Tumor Necrosis ◽  
Fluorescent Protein ◽  
Tumor Necrosis Factor Receptor ◽  
Negative Regulator ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Necrosis Factor

Stroke induced by middle cerebral artery occlusion leads to transiently increased progenitor proliferation in the subventricular zone (SVZ) and long-lasting striatal neurogenesis in adult rodents. Tumor necrosis factor-α (TNF-α) is upregulated in stroke-damaged brain. Whether TNF-α and its receptors influence SVZ progenitor proliferation after stroke is unclear. Here we show that the increased proliferation 1 week after stroke occurred concomitantly with elevated microglia numbers and TNF-α and TNF receptor-1 (TNF-R1) gene expression in the SVZ of wild-type mice. TNF receptor-1 was expressed on sorted SVZ progenitor cells from nestin-green fluorescent protein reporter mice. In animals lacking TNF-R1, stroke-induced SVZ cell proliferation and neuroblast formation were enhanced. In contrast, deletion of TNF-R1 did not alter basal or status epilepticus-stimulated cell proliferation in SVZ. Addition of TNF-α reduced the size and numbers of SVZ neurospheres through a TNF-R1-dependent mechanism without affecting cell survival. Our results provide the first evidence that TNF-R1 is a negative regulator of stroke-induced SVZ progenitor proliferation. Blockade of TNF-R1 signaling might be a novel strategy to promote the proliferative response in SVZ after stroke.

scholarly journals Tumor necrosis factor receptor-associated factor-1 enhances proinflammatory TNF receptor-2 signaling and modifies TNFR1–TNFR2 cooperation

Oncogene ◽  
2009 ◽  
Vol 28 (15) ◽  
pp. 1769-1781 ◽  
Author(s):  
A Wicovsky ◽  
F Henkler ◽  
S Salzmann ◽  
P Scheurich ◽  
C Kneitz ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Tnf Receptor ◽  
Associated Factor ◽  
Necrosis Factor
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