scholarly journals An in Vivo Model for Elucidation of the Mechanism of Tumor Necrosis Factor-α (TNF-α)-Induced Insulin Resistance: Evidence for Differential Regulation of Insulin Signaling by TNF-α

Endocrinology ◽  
1998 ◽  
Vol 139 (12) ◽  
pp. 4928-4935 ◽  
Author(s):  
Anthony T. Cheung ◽  
Daniel Ree ◽  
Jay K. Kolls ◽  
Joseph Fuselier ◽  
David H. Coy ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Signaling ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Differential Regulation ◽  
In Vivo Model ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Combined anticoagulant and antiselectin treatments prevent lethal intravascular coagulation

Blood ◽  
2003 ◽  
Vol 101 (3) ◽  
pp. 921-928 ◽  
Author(s):  
Keith E. Norman ◽  
Matthew J. Cotter ◽  
James B. Stewart ◽  
Kate B. Abbitt ◽  
Majid Ali ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Platelet Adhesion ◽  
Traumatic Shock ◽  
Intravascular Coagulation ◽  
Tnf Α ◽  
Factor Α ◽  
Blocking Antibodies ◽  
Necrosis Factor

AbstractWidespread microvascular injury followed by vessel obstruction may lead to disseminated intravascular coagulation (DIC). We describe a murine model wherein leukocytes interacting with inflamed microvessels in vivo are activated by antibodies. Treatment of tumor necrosis factor α (TNF-α)–primed mice with anti–Ly-6G antibodies reproduced many of the features of septic or traumatic shock including microvessel obstruction and coagulation, severe vasculitis, respiratory difficulties, and vascular leakage. Mice lacking either E-selectin or P-selectin were protected from this reaction as were animals treated with a combination of either selectin-blocking antibodies and heparin or a selectin antagonist plus heparin. Combined blockade of leukocyte/platelet adhesion and coagulation may provide convincing protection in DIC.

scholarly journals Tumor necrosis factor α (TNF-α) receptor-II is required for TNF-α–induced leukocyte-endothelial interaction in vivo

Blood ◽  
2006 ◽  
Vol 109 (5) ◽  
pp. 1938-1944 ◽  
Author(s):  
Unni M. Chandrasekharan ◽  
Maria Siemionow ◽  
Murat Unsal ◽  
Lin Yang ◽  
Earl Poptic ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Leukocyte Adhesion ◽  
Leukocyte Rolling ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Leukocyte Adhesion Molecules

Abstract Tumor necrosis factor-α (TNF-α) binds to 2 distinct cell-surface receptors: TNF-α receptor-I (TNFR-I: p55) and TNF-α receptor-II (TNFR-II: p75). TNF-α induces leukocyte adhesion molecules on endothelial cells (ECs), which mediate 3 defined steps of the inflammatory response; namely, leukocyte rolling, firm adhesion, and transmigration. In this study, we have investigated the role of p75 in TNF-α–induced leukocyte adhesion molecules using cultured ECs derived from wild-type (WT), p75-null (p75−/−), or p55-null (p55−/−) mice. We observed that p75 was essential for TNF-α–induced E-selectin, vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) expression. We also investigated the putative role of p75 in inflammation in vivo using an intravital microscopic approach with a mouse cremaster muscle model. TNF-α–stimulated leukocyte rolling, firm adhesion to ECs, and transmigration were dramatically reduced in p75−/− mice. Transplanted WT cremaster in p75−/− mice showed a robust leukocyte rolling and firm adhesion upon TNF-α activation, suggesting that the impairment in EC-leukocyte interaction in p75−/− mice is due to EC dysfunction. These results demonstrate, for the first time, that endothelial p75 is essential for TNF-α–induced leukocyte–endothelial-cell interaction. Our findings may contribute to the identification of novel p75-targeted therapeutic approaches for inflammatory diseases.

The adipose triglyceride lipase, adiponectin and visfatin are downregulated by tumor necrosis factor-α (TNF-α) in vivo

Cytokine ◽  
2009 ◽  
Vol 45 (1) ◽  
pp. 12-19 ◽  
Author(s):  
Ling Li ◽  
Gangyi Yang ◽  
Shaochuan Shi ◽  
Mengliu Yang ◽  
Hua Liu ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor
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