SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy.
Progressive reduction of SnoN is associated with gradual elevation of TGF-β1 during diabetic nephropathy progression, suggesting SnoN to be a possible mediator of TGF-β1 signaling, with potential therapeutic benefits against TGF- β1 -induced renal fibrosis. To characterize SnoN for its role in renal...
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doaj-528ee5f3def44a7784ed8b9bc27e592e2020-11-24T21:40:56ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01123e017447110.1371/journal.pone.0174471SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy.Lirong LiuMingjun ShiYuanyuan WangChangzhi ZhangBo SuYing XiaoBing GuoProgressive reduction of SnoN is associated with gradual elevation of TGF-β1 during diabetic nephropathy progression, suggesting SnoN to be a possible mediator of TGF-β1 signaling, with potential therapeutic benefits against TGF- β1 -induced renal fibrosis. To characterize SnoN for its role in renal fibrosis, we assessed SnoN expression patterns in response to high glucose stress, and evaluated the effects of upregulating SnoN on renal fibrosis. High glucose stress induced significantly elevated SnoN, TGF-β1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions. Upregulating the SnoN protein was achieved by Arkadia knockdown, which resulted in inhibited high glucose-induced epithelial-mesenchymal transition (EMT) in renal tubular cells, the onset phase of renal fibrosis. Alternatively, EMT was suppressed by dominantly expressed exogenous SnoN without interfering with TGF-β1. Overall, renal SnoN upregulation ameliorates renal fibrosis by relieving high glucose-induced EMT; these findings support a translational approach targeting SnoN for the treatment of diabetic nephropathy.http://europepmc.org/articles/PMC5370123?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lirong Liu Mingjun Shi Yuanyuan Wang Changzhi Zhang Bo Su Ying Xiao Bing Guo |
spellingShingle |
Lirong Liu Mingjun Shi Yuanyuan Wang Changzhi Zhang Bo Su Ying Xiao Bing Guo SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy. PLoS ONE |
author_facet |
Lirong Liu Mingjun Shi Yuanyuan Wang Changzhi Zhang Bo Su Ying Xiao Bing Guo |
author_sort |
Lirong Liu |
title |
SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy. |
title_short |
SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy. |
title_full |
SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy. |
title_fullStr |
SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy. |
title_full_unstemmed |
SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy. |
title_sort |
snon upregulation ameliorates renal fibrosis in diabetic nephropathy. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2017-01-01 |
description |
Progressive reduction of SnoN is associated with gradual elevation of TGF-β1 during diabetic nephropathy progression, suggesting SnoN to be a possible mediator of TGF-β1 signaling, with potential therapeutic benefits against TGF- β1 -induced renal fibrosis. To characterize SnoN for its role in renal fibrosis, we assessed SnoN expression patterns in response to high glucose stress, and evaluated the effects of upregulating SnoN on renal fibrosis. High glucose stress induced significantly elevated SnoN, TGF-β1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions. Upregulating the SnoN protein was achieved by Arkadia knockdown, which resulted in inhibited high glucose-induced epithelial-mesenchymal transition (EMT) in renal tubular cells, the onset phase of renal fibrosis. Alternatively, EMT was suppressed by dominantly expressed exogenous SnoN without interfering with TGF-β1. Overall, renal SnoN upregulation ameliorates renal fibrosis by relieving high glucose-induced EMT; these findings support a translational approach targeting SnoN for the treatment of diabetic nephropathy. |
url |
http://europepmc.org/articles/PMC5370123?pdf=render |
work_keys_str_mv |
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