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-β1 Signaling Pathway

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. Result...

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Main Authors: Zhiqin Liu, Leixi Xue, Zhichun Liu, Jun Huang, Jian Wen, Ji Hu, Lin Bo, Ru Yang
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2016/8986451
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author Zhiqin Liu
Leixi Xue
Zhichun Liu
Jun Huang
Jian Wen
Ji Hu
Lin Bo
Ru Yang
author_facet Zhiqin Liu
Leixi Xue
Zhichun Liu
Jun Huang
Jian Wen
Ji Hu
Lin Bo
Ru Yang
author_sort Zhiqin Liu
collection DOAJ
description 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-β1, p-p38 MAPK, p-Smad2, COL-1, and α-SMA proteins. In vitro, hTWEAK treatment upregulated the expressions of TGF-β1, p-p38 MAPK, p-SMAD2, α-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-β1 signaling pathway, and phosphorylation of Smad2 and p38 MAPK proteins was also involved in this signaling pathway.
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institution Kabale University
issn 0962-9351
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publishDate 2016-01-01
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series Mediators of Inflammation
spelling doaj-art-08493d65f2c74608b9182b25f4e5a55a2025-08-20T03:55:32ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/89864518986451Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Accelerates the Progression of Renal Fibrosis in Lupus Nephritis by Activating SMAD and p38 MAPK in TGF-β1 Signaling PathwayZhiqin Liu0Leixi Xue1Zhichun Liu2Jun Huang3Jian Wen4Ji Hu5Lin Bo6Ru Yang7Department of Biological Science & Engineering, Hebei University of Science & Technology, Shijiazhuang 050018, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, ChinaThis 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-β1, p-p38 MAPK, p-Smad2, COL-1, and α-SMA proteins. In vitro, hTWEAK treatment upregulated the expressions of TGF-β1, p-p38 MAPK, p-SMAD2, α-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-β1 signaling pathway, and phosphorylation of Smad2 and p38 MAPK proteins was also involved in this signaling pathway.http://dx.doi.org/10.1155/2016/8986451
spellingShingle Zhiqin Liu
Leixi Xue
Zhichun Liu
Jun Huang
Jian Wen
Ji Hu
Lin Bo
Ru Yang
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-β1 Signaling Pathway
Mediators of Inflammation
title 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-β1 Signaling Pathway
title_full 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-β1 Signaling Pathway
title_fullStr 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-β1 Signaling Pathway
title_full_unstemmed 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-β1 Signaling Pathway
title_short 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-β1 Signaling Pathway
title_sort 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 β1 signaling pathway
url http://dx.doi.org/10.1155/2016/8986451
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