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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&amp;3p, and STAT3. In cultured human kidney tubular epithelial cells (HK-2), TGF-\u03b21 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-\u03b1 blocked STAT3 activation and the expression of miR-199a-3p, collagen I, and vimentin during TGF-\u03b21 treatment. Over-expression of miR-199a-3p increased TGF\u03b21-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.<\/jats:p>","DOI":"10.1038\/srep43409","type":"journal-article","created":{"date-parts":[[2017,2,27]],"date-time":"2017-02-27T11:07:10Z","timestamp":1488193630000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":84,"title":["p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO"],"prefix":"10.1038","volume":"7","author":[{"given":"Ruhao","family":"Yang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuan","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huiling","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinwen","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xudong","family":"Xiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zheng","family":"Dong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongshan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,2,27]]},"reference":[{"key":"BFsrep43409_CR1","doi-asserted-by":"crossref","unstructured":"Schieppati, A. & Remuzzi, G. 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