The Angiotensin II Type 1 Receptor Mediates Renal Interstitial Content of Tumor Necrosis Factor-α in Diabetic Rats

Diabetes with vascular complication needs strict interventions to retard possible serious complications. This research estimated the possible interaction of rosiglitazone (RGN) with losartan (Los) in diabetic rats. Male Sprague–Dawley rats were randomly divided into nondiabetic rats, diabetic rats, and diabetic rats that received RGN, Los, or a combination of RGN and Los. Measurement of serum glucose, vascular adhesion molecule-1, interleukin-6, tumor necrosis factor-α, aortic lipid peroxide (malondialdehyde), glutathione, superoxide dismutase, and total nitrate/nitrite levels was done. Also, the effects of RGN on the relaxation created by acetylcholine and sodium nitroprusside, contraction of isolated aortic rings provoked by phenylephrine and angiotensin II were determined. Results revealed that RGN or Los had a vasodilating effect to variable degrees indicated by enhanced effects on both acetylcholine-induced relaxation and the antagonistic effect on angiotensin II and phenylephrine-stimulated contraction of diabetic aortas with significant amelioration in serum glucose, vascular adhesion molecule-1, interleukin-6, and tumor necrosis factor-α levels and aortic oxidant/antioxidant balance. Treatment of diabetic rats with a combination of RGN and Los produced a more pronounced effect on the measured parameters compared to the diabetic, RGN-, and Los-treated groups. These findings point out the beneficial effects of RGN and Los combination in diabetic rats.

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Tumor Necrosis Factor-α Upregulates Angiotensin II Type 1 Receptors on Cardiac Fibroblasts

Circulation Research ◽

10.1161/01.res.85.3.272 ◽

1999 ◽

Vol 85 (3) ◽

pp. 272-279 ◽

Cited By ~ 67

Author(s):

Devorah Gurantz ◽

Randy T. Cowling ◽

Francisco J. Villarreal ◽

Barry H. Greenberg

Keyword(s):

Angiotensin Ii ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Cardiac Fibroblasts ◽

Factor Α ◽

Necrosis Factor

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Transcription Factor NF-κB Is Necessary for Up-regulation of Type 1 Angiotensin II Receptor mRNA in Rat Cardiac Fibroblasts Treated with Tumor Necrosis Factor-α or Interleukin-1β

Journal of Biological Chemistry ◽

10.1074/jbc.m107515200 ◽

2001 ◽

Vol 277 (8) ◽

pp. 5719-5724 ◽

Cited By ~ 60

Author(s):

Randy T. Cowling ◽

Devorah Gurantz ◽

JianFeng Peng ◽

Wolfgang H. Dillmann ◽

Barry H. Greenberg

Keyword(s):

Transcription Factor ◽

Angiotensin Ii ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Cardiac Fibroblasts ◽

Angiotensin Ii Receptor ◽

Receptor Mrna ◽

Factor Α ◽

Necrosis Factor

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Tumor Necrosis Factor α Is Associated With Viral Control and Early Disease Progression in Patients With HIV Type 1 Infection

The Journal of Infectious Diseases ◽

10.1093/infdis/jiu206 ◽

2014 ◽

Vol 210 (7) ◽

pp. 1042-1046 ◽

Cited By ~ 21

Author(s):

Sagar A. Vaidya ◽

Christian Korner ◽

Michael N. Sirignano ◽

Molly Amero ◽

Sue Bazner ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Disease Progression ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Early Disease ◽

Viral Control ◽

Hiv Type 1 ◽

Factor Α ◽

Necrosis Factor

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Contributions of angiotensin II and tumor necrosis factor-α to the development of renal fibrosis

AJP Renal Physiology ◽

10.1152/ajprenal.2001.280.5.f777 ◽

2001 ◽

Vol 280 (5) ◽

pp. F777-F785 ◽

Cited By ~ 87

Author(s):

Guangjie Guo ◽

Jeremiah Morrissey ◽

Ruth McCracken ◽

Timothy Tolley ◽

Helen Liapis ◽

...

Keyword(s):

Angiotensin Ii ◽

Tumor Necrosis Factor ◽

Renal Fibrosis ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Wild Type ◽

Tnf Α ◽

Factor Α ◽

Tgf Β1 ◽

Necrosis Factor

Angiotensin II upregulates tumor necrosis factor-α (TNF-α) in the rat kidney with unilateral ureteral obstruction (UUO). In a mouse model of UUO, we found that tubulointerstitial fibrosis is blunted when the TNF-α receptor, TNFR1, is functionally knocked out. In this study, we used mutant mice with UUO in which the angiotensin II receptor AT1a or the TNF-α receptors TNFR1 and TNFR2 were knocked out to elucidate interactions between the two systems. The contribution of both systems to renal fibrosis was assessed by treating TNFR1/TNFR2-double knockout (KO) mice with an angiotensin-converting enzyme inhibitor, enalapril. The increased interstitial volume (Vvint) in the C57BI/6 wild-type mouse was decreased in the AT1a KO from 32.8 ± 4.0 to 21.0 ± 3.7% ( P < 0.005) or in the TNFR1/TNFR2 KO to 22.3 ± 2.1% ( P < 0.005). The Vvint of the TNFR1/TNFR2 KO was further decreased to 15.2 ± 3.7% ( P < 0.01) by enalapril compared with no treatment. The induction of TNF-α mRNA and transforming growth factor-β1 (TGF-β1) mRNA in the kidney with UUO was significantly blunted in the AT1a or TNFR1/TNFR2 KO mice compared with the wild-type mice. Treatment of the TNFR1/TNFR2 KO mouse with enalapril reduced both TNF-α and TGF-β1 mRNA and their proteins to near normal levels. Also, α-smooth muscle actin expression and myofibroblast proliferation were significantly inhibited in the AT1a or TNFR1/TNFR2 KO mice, and they were further inhibited in enalapril-treated TNFR1/TNFR2 KO mice. Incapacitating the angiotensin II or the TNF-α systems individually leads to partial blunting of fibrosis. Incapacitating both systems, by using a combination of genetic and pharmacological means, further inhibited interstitial fibrosis and tubule atrophy in obstructive nephropathy.

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