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10.1038/srep43409 http://scihub22266oqcxt.onion/10.1038/srep43409 C5327480!5327480!28240316     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28240316|t=2017. p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO |pdf=|usr=}}{{28240316}} gab.com Text p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28240316 #FOAvip The role of p53 in renal fibrosis has recently been suggested, however, its function remains controversial and the underlying mechanism is unclear. Here, we show that pharmacological and genetic blockade of p53 attenuated renal interstitial fibrosis, apoptosis, and inflammation in mice with unilateral urethral obstruction (UUO). Interestingly, p53 blockade was associated with the suppression of miR-215-5p, miR-199a-5p&3p, and STAT3. In cultured human kidney tubular epithelial cells (HK-2), TGF-?1 treatment induced fibrotic changes, including collagen I and vimentin expression, being associated with p53 accumulation, p53 Ser15 phosphorylation, and miR-199a-3p expression. Inhibition of p53 by pifithrin-? blocked STAT3 activation and the expression of miR-199a-3p, collagen I, and vimentin during TGF-?1 treatment. Over-expression of miR-199a-3p increased TGF?1-induced collagen I and vimentin expression and restored SOCS7 expression. Furthermore, SOCS7 was identified as a target gene of miR-199a-3p, and silencing of SOCS7 promoted STAT3 activation. ChIp analyses indicated the binding of p53 to the promoter region of miR-199a-3p. Consistently, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of p53 and STAT3, decreased expression of SOCS7, and increase in profibrotic proteins and miR-199a-3p. Together, these results demonstrate the novel p53/miR-199a-3p/SOCS7/STAT3 pathway in renal interstitial fibrosis. Twit Text FOAVip p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28240316 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28240316 #FOAvip English Wikipedia <ref>{{Cite pmid|28240316}}</ref> p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO #MMPMID28240316 Yang R; Xu X; Li H; Chen J; Xiang X; Dong Z; Zhang D Sci Rep 2017[]; 7 (ä): ä PMID28240316show ga The role of p53 in renal fibrosis has recently been suggested, however, its function remains controversial and the underlying mechanism is unclear. Here, we show that pharmacological and genetic blockade of p53 attenuated renal interstitial fibrosis, apoptosis, and inflammation in mice with unilateral urethral obstruction (UUO). Interestingly, p53 blockade was associated with the suppression of miR-215-5p, miR-199a-5p&3p, and STAT3. In cultured human kidney tubular epithelial cells (HK-2), TGF-?1 treatment induced fibrotic changes, including collagen I and vimentin expression, being associated with p53 accumulation, p53 Ser15 phosphorylation, and miR-199a-3p expression. Inhibition of p53 by pifithrin-? blocked STAT3 activation and the expression of miR-199a-3p, collagen I, and vimentin during TGF-?1 treatment. Over-expression of miR-199a-3p increased TGF?1-induced collagen I and vimentin expression and restored SOCS7 expression. Furthermore, SOCS7 was identified as a target gene of miR-199a-3p, and silencing of SOCS7 promoted STAT3 activation. ChIp analyses indicated the binding of p53 to the promoter region of miR-199a-3p. Consistently, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of p53 and STAT3, decreased expression of SOCS7, and increase in profibrotic proteins and miR-199a-3p. Together, these results demonstrate the novel p53/miR-199a-3p/SOCS7/STAT3 pathway in renal interstitial fibrosis. äp53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and rena(epmc).pdf DeepDyve Pubget Overpricing