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10.1155/2018/1031367

http://scihub22266oqcxt.onion/10.1155/2018/1031367
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C6040246!6040246!30050950
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suck abstract from ncbi


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pmid30050950      J+Diabetes+Res 2018 ; 2018 (ä): ä
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  • Metformin Improves Epithelial-to-Mesenchymal Transition Induced by TGF-?1 in Renal Tubular Epithelial NRK-52E Cells via Inhibiting Egr-1 #MMPMID30050950
  • Guan M; Li W; Xu L; Zeng Y; Wang D; Zheng Z; Lyv F; Xue Y
  • J Diabetes Res 2018[]; 2018 (ä): ä PMID30050950show ga
  • The early growth response- (Egr-) 1 has been found to play a key role in organ fibrosis. Metformin has been shown to be effective in attenuating renal tubular epithelial-to-mesenchymal transition (EMT), which is involved in renal fibrosis. However, it is unknown whether metformin improves EMT via inhibiting Egr-1. In this study, rat renal tubular epithelial (NRK-52 E) cells, treated by transforming growth factor- (TGF-) ?1 of 10?ng/ml with or without metformin of 1?mmol/l, were transfected by siEgr-1 or M61-Egr-1 plasmids to knock down or overexpress Egr-1, respectively. The gene and protein expressions of E-cadherin, ?-SMA, fibronectin (FN), and Egr-1 were determined by real-time quantitative PCR and Western blotting, respectively. We observed that TGF-?1 significantly reduced E-cadherin expression and upregulated the expressions of FN, ?-SMA, and Egr-1, which can be reversed by metformin. M61-Egr-1 transfection could exacerbate EMT, which can be reversed by metformin. Taken together, our data show that Egr-1 plays an important role in TGF-?1-induced EMT of renal tubular epithelial cells and metformin improves EMT while inhibiting Egr-1, which provides a potential novel target to combat renal fibrosis.
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