High Glucose Induces Sumoylation of Smad4 via SUMO2/3 in Mesangial Cells

Recent studies have shown that sumoylation is a posttranslational modification involved in regulation of the transforming growth factor-β (TGF-β) signaling pathway, which plays a critical role in renal fibrosis in diabetic nephropathy (DN). However, the role of sumoylation in the regulation of TGF-β...

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Bibliographic Details
Published in:BioMed research international 2014-01, Vol.2014 (2014), p.1-10
Main Authors: Zhou, Xueqin, Gao, Chenlin, Huang, Wei, Yang, Maojun, Chen, Guo, Jiang, Lan, Gou, Fang, Feng, Hong, Ai, Na, Xu, Yong
Format: Article
Language:English
Subjects:
Animals
Blood sugar
Cell Line
Diabetes
Diabetic nephropathies
DNA repair
Enzymes
Fibronectins - genetics
Fibronectins - metabolism
Gene Expression Regulation
Glucose - pharmacology
Hospitals
Mesangial Cells - drug effects
Mesangial Cells - metabolism
Neurosciences
Pathogenesis
Physiological aspects
Post-translational modification
Protein Transport - drug effects
Proteins
Rats
Reverse Transcriptase Polymerase Chain Reaction
Risk factors
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Signal transduction
Smad4 Protein - metabolism
Small Ubiquitin-Related Modifier Proteins - genetics
Small Ubiquitin-Related Modifier Proteins - metabolism
Studies
Sumoylation - drug effects
Transforming growth factors
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Summary:Recent studies have shown that sumoylation is a posttranslational modification involved in regulation of the transforming growth factor-β (TGF-β) signaling pathway, which plays a critical role in renal fibrosis in diabetic nephropathy (DN). However, the role of sumoylation in the regulation of TGF-β signaling in DN is still unclear. In the present study, we investigated the expression of SUMO (SUMO1 and SUMO2/3) and Smad4 and the interaction between SUMO and Smad4 in cultured rat mesangial cells induced by high glucose. We found that SUMO1 and SUMO2/3 expression was significantly increased in the high glucose groups compared to the normal group P
ISSN:2314-6133
2314-6141
DOI:10.1155/2014/782625