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[High glucose induces sumoylation of Smad4 via SUMO2/3 in glomerular mesangial cells].

Authors: Zhou, Xue-qin  Huang, Wei  Xu, Yong  Yang, Mao-jun 
Citation: Zhou XQ, etal., Sichuan Da Xue Xue Bao Yi Xue Ban. 2014 May;45(3):380-5.
Pubmed: (View Article at PubMed) PMID:24941801


OBJECTIVE: To investigate the expression of SUMO2/3 and Smad4 in rat glomerular mesangial cells (GMCs) induced by high glucose, and the interaction between small ubiquitin related modifier (SUMO)2/3 and Smad4; and to explore the role and mechanism of sumoylation in regulating TGF-p signaling in diabetic nephropathy.
METHODS: Cultured rat GMCs were divided into five groups: normal glucose group (5. 6 mmol/L glucose), high glucose groups (10, 20 and 30 mmol/L glucose), and mannitol group (osmotic control). The expression of SUMO2/3, Smad4 and fibronectin (FN) was measured by Western blot and RT-PCR. The interaction and colocalization between SUMO2/3 and Smad4 were detected by Co-immunoprecipitation and immunofluorescence confocal laser microscopy.
RESULTS: Compared with controls, the expressions of SUMO2/3, Smad4 and FN in the cells in the high glucose groups increased (P < 0.05). The co-immunoprecipitation and immunofluorescence confocal laser scanning showed that Smad4 interacted and colocalized with SUMO2/3 and the sumolyation (SUMO2/3) of Smad4 was enhanced significantly in the high glucose groups compared with the control group (P < 0.05).
CONCLUSION: Sumolyation of Samd4 by SUMO2/3 may be involved in the regulation of TGF-beta signaling in diabetic nephropathy.

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CRRD Object Information
CRRD ID: 12880051
Created: 2017-05-02
Species: All species
Last Modified: 2017-05-02
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.