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| MiR-302b suppresses the high-sucrose induced pithelial-mesenchymal transition in diabetic nephropathy |
| ZHANG Chengjie, ZHENG Yuming, CHEN Guiyan |
| Department of Emergency,Binzhou People's Hospital,Binzhou 256610,P.R.China |
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Abstract Objective Diabetic nephropathy (DN) is a kind of vascular complication for diabetes, and its pathogenesis remains complicate.This study aimed to investigate the potential role of miR-302b in the high-sucrose induced epithelial-mesenchymal transition (EMT) during the development of DN and to reveal its possible molecular mechanism.Methods The podocytes and epithelial cells were treated with the high-sucrose (30 mM) to construct the DN model.The overexpressed vector of miR-302b was packaged by the virus packaging method and then was transfected into the podocytes and epithelial cells.Results The EMT-related protein including slug,snail,vimentin and fibronectin was significantly decreased,whereas E-cadherin,β-catenin and α-catenin were significantly increased by the overexpression of miR-302b.Conclusion Taken together, our study revealed that the overexpression of miR-302b functioned as a protector in the development of DN by suppressing the high-sucrose induced EMT process.
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Received: 17 April 2018
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