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10.1155/2016/8986451

http://scihub22266oqcxt.onion/10.1155/2016/8986451
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C4913011!4913011!27365897
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suck abstract from ncbi


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pmid27365897      Mediators+Inflamm 2016 ; 2016 (ä): ä
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  • Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Accelerates the Progression of Renal Fibrosis in Lupus Nephritis by Activating SMAD and p38 MAPK in TGF-?1 Signaling Pathway #MMPMID27365897
  • Liu Z; Xue L; Liu Z; Huang J; Wen J; Hu J; Bo L; Yang R
  • Mediators Inflamm 2016[]; 2016 (ä): ä PMID27365897show ga
  • This study aim was to explore the effects of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in lupus nephritis and its potential underlying mechanisms. MRL/lpr mice were used for in vivo experiments and human proximal tubular cells (HK2 cells) were used for in vitro experiments. Results showed that MRL/lpr mice treated with vehicle solution or LV-Control shRNA displayed significant proteinuria and severe renal histopathological changes. LV-TWEAK-shRNA treatment reversed these changes and decreased renal expressions of TWEAK, TGF-?1, p-p38 MAPK, p-Smad2, COL-1, and ?-SMA proteins. In vitro, hTWEAK treatment upregulated the expressions of TGF-?1, p-p38 MAPK, p-SMAD2, ?-SMA, and COL-1 proteins in HK2 cells and downregulated the expressions of E-cadherin protein, which were reversed by cotreatment with anti-TWEAK mAb or SB431542 treatment. These findings suggest that TWEAK may contribute to chronic renal changes and renal fibrosis by activating TGF-?1 signaling pathway, and phosphorylation of Smad2 and p38 MAPK proteins was also involved in this signaling pathway.
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