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. 2016 Apr 27;7(24):36510–36528. doi: 10.18632/oncotarget.9058

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Copyright: © 2016 Bai et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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A, B. Expression levels of CDK5, p35, phosphorylated ERK and PPARγ, E-cadherin, Vimentin and Collagen IV in microdissected renal tubules compared between groups. C. A schematic illustration showing that roscovitine inhibited DN progression through dampening the EMT process and fibrosis via the ERK1/2/PPARγ pathway. Results are presented as mean ± SD for groups of 6-9 rats of three independent experiments. *P<0.05, #P<0.001. NC-D, normal control rats treated with dimethyl sulphoxide; NC-R, normal control rats treated with roscovitine; DM-D, diabetic rats treated with dimethyl sulphoxide; DM-R, diabetic rats treated with roscovitine; EMT, epithelial-to-mesenchymal transition; DN, diabetic nephropathy. , NC-D; , NC-R; , DM-D; , DM-R.

Inline graphic — A, B. Expression levels of CDK5, p35, phosphorylated ERK and PPARγ, E-cadherin, Vimentin and Collagen IV in microdissected renal tubules compared between groups. C. A schematic illustration showing that roscovitine inhibited DN progression through dampening the EMT process and fibrosis via the ERK1/2/PPARγ pathway. Results are presented as mean ± SD for groups of 6-9 rats of three independent experiments. *P<0.05, #P<0.001. NC-D, normal control rats treated with dimethyl sulphoxide; NC-R, normal control rats treated with roscovitine; DM-D, diabetic rats treated with dimethyl sulphoxide; DM-R, diabetic rats treated with roscovitine; EMT, epithelial-to-mesenchymal transition; DN, diabetic nephropathy. , NC-D; , NC-R; , DM-D; , DM-R.