ASSOCIATION OF TUMOR NECROSIS FACTOR α, INTERLEUKIN 6, AND INTERLEUKIN 10 PROMOTER POLYMORPHISM WITH PROLIFERATIVE DIABETIC RETINOPATHY IN TYPE 2 DIABETIC SUBJECTS

Retina ◽  
2012 ◽  
Vol 32 (6) ◽  
pp. 1197-1203 ◽  
Author(s):  
Suman K. Paine ◽  
Aditi Sen ◽  
Subhadip Choudhuri ◽  
Lakshmi K. Mondal ◽  
Imran H. Chowdhury ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Promoter Polymorphism ◽  
Factor Α ◽  
Type 2 Diabetic ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) −863C/A promoter polymorphism is associated with type 2 diabetes in Tunisian population

2013 ◽  
Vol 102 (2) ◽  
pp. e24-e28 ◽  
Author(s):  
Amani Kallel ◽  
Bochra Ftouhi ◽  
Zeineb Jemaa ◽  
Imen Mahjoubi ◽  
Moncef Feki ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Promoter Polymorphism ◽  
Tunisian Population ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Effects of Tumor Necrosis Factor-α on Glucose Metabolism in Cultured Human Muscle Cells from Nondiabetic and Type 2 Diabetic Subjects1

Endocrinology ◽  
1998 ◽  
Vol 139 (12) ◽  
pp. 4793-4800 ◽  
Author(s):  
Theodore P. Ciaraldi ◽  
Leslie Carter ◽  
Sunder Mudaliar ◽  
Philip A. Kern ◽  
Robert R. Henry
Keyword(s):  
Tumor Necrosis Factor ◽  
Glucose Metabolism ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Muscle ◽  
Factor Α ◽  
Human Muscle Cells ◽  
Type 2 Diabetic ◽  
Necrosis Factor

scholarly journals The Influence of Tumor Necrosis Factor–α and Interleukin‐10 Gene Promoter Polymorphism on the Inflammatory Response in Experimental Human Endotoxemia

2001 ◽  
Vol 33 (9) ◽  
pp. 1601-1603 ◽  
Author(s):  
J. W. Fijen ◽  
J. E. Tulleken ◽  
B. G. Hepkema ◽  
T. S. van der Werf ◽  
J. J. M. Ligtenberg ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gene Promoter ◽  
Interleukin 10 ◽  
Promoter Polymorphism ◽  
Human Endotoxemia ◽  
Factor Α ◽  
Necrosis Factor ◽  
Gene Promoter Polymorphism

Adjuvant-Induced Improvement of Glucose Intolerance in Type 2 Diabetic KK-Ay Mice Through Interleukin-1 and Tumor Necrosis Factor-α

2000 ◽  
Vol 97 (3) ◽  
pp. 259-265 ◽  
Author(s):  
Gen Muto ◽  
Jo Satoh ◽  
Yoshiko Muto ◽  
Kazuma Takahashi ◽  
Tetsuya Nakazawa ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Glucose Intolerance ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1 ◽  
Factor Α ◽  
Type 2 Diabetic ◽  
Necrosis Factor ◽  
Ay Mice

scholarly journals Targeted Deletion of Class A Macrophage Scavenger Receptor Increases the Risk of Cardiac Rupture After Experimental Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1904-1911 ◽  
Author(s):  
Kenichi Tsujita ◽  
Koichi Kaikita ◽  
Takanori Hayasaki ◽  
Tsuyoshi Honda ◽  
Hironori Kobayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Experimental Myocardial Infarction ◽  
Cardiac Rupture ◽  
Infarcted Myocardium ◽  
Factor Α ◽  
Necrosis Factor

Background— Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A–deficient (SR-A −/− ) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Methods and Results— Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A −/− and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A −/− mice than in WT mice ( P =0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A −/− mice and 12% (6 of 51 mice) in WT mice ( P =0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A −/− mice compared with WT mice. Real-time reverse transcription–polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A −/− mice compared with WT mice. Furthermore, SR-A −/− mice showed augmented expression of tumor necrosis factor-α and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-α and decreased interleukin-10 expression in activated SR-A −/− macrophages. Conclusions— The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-α and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

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