Tumor Necrosis Factor Superfamily 14 Is Essential for Renal Fibrosis via Potentiating Sphingosine Kinase-1 Expression

2019 ◽  
Author(s):  
You Li ◽  
Ming Tang ◽  
Xu Cao ◽  
Feng Xu ◽  
Kun Zhang ◽  
...  
Aging ◽  
2020 ◽  
Author(s):  
You Li ◽  
Ming Tang ◽  
Bo Han ◽  
Shun Wu ◽  
Shu-jing Li ◽  
...  

2005 ◽  
Vol 280 (17) ◽  
pp. 17196-17202 ◽  
Author(s):  
Tarek A. Taha ◽  
Kazuyuki Kitatani ◽  
Jacek Bielawski ◽  
Wonhwa Cho ◽  
Yusuf A. Hannun ◽  
...  

FEBS Letters ◽  
2007 ◽  
Vol 581 (23) ◽  
pp. 4384-4388 ◽  
Author(s):  
Chiara Donati ◽  
Paola Nincheri ◽  
Francesca Cencetti ◽  
Elena Rapizzi ◽  
Marta Farnararo ◽  
...  

2001 ◽  
Vol 280 (5) ◽  
pp. F777-F785 ◽  
Author(s):  
Guangjie Guo ◽  
Jeremiah Morrissey ◽  
Ruth McCracken ◽  
Timothy Tolley ◽  
Helen Liapis ◽  
...  

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.


1999 ◽  
Vol 274 (24) ◽  
pp. 16773-16781 ◽  
Author(s):  
Roberto Doliana ◽  
Maurizio Mongiat ◽  
Francesco Bucciotti ◽  
Emiliana Giacomello ◽  
Rainer Deutzmann ◽  
...  

2017 ◽  
Author(s):  
Christian Gieffers ◽  
Christian Merz ◽  
David Richards ◽  
Mauricio Redondo ◽  
Viola Marschall ◽  
...  

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