{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,20]],"date-time":"2026-06-20T05:20:04Z","timestamp":1781932804051,"version":"3.54.5"},"reference-count":41,"publisher":"Portland Press Ltd.","issue":"6","license":[{"start":{"date-parts":[[2020,6,2]],"date-time":"2020-06-02T00:00:00Z","timestamp":1591056000000},"content-version":"vor","delay-in-days":1,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,6,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Diabetic nephropathy (DN) commonly causes end-stage renal disease (ESRD). Increasing evidence indicates that abnormal miRNA expression is tightly associated with chronic kidney disease (CKD). This work aimed to investigate whether miR-27a can promote the occurrence of renal fibrosis in DN by suppressing the expression of secreted frizzled-related protein 1 (Sfrp1) to activate Wnt\/\u03b2-catenin signalling. Therefore, we assessed the expression levels of miR-27a, Sfrp1, Wnt signalling components, and extracellular matrix (ECM)-related molecules in vitro and in vivo. Sfrp1 was significantly down-regulated in a high-glucose environment, while miR-27a levels were markedly increased. A luciferase reporter assay confirmed that miR-27a down-regulated Sfrp1 by binding to the 3\u2032 untranslated region directly. Further, NRK-52E cells under high-glucose conditions underwent transfection with miR-27a mimic or the corresponding negative control, miR-27a inhibitor or the corresponding negative control, si-Sfrp1, or combined miR-27a inhibitor and si-Sfrp1. Immunoblotting and immunofluorescence were performed to assess the relative expression levels of Wnt\/\u03b2-catenin signalling and ECM components. The mRNA levels of Sfrp1, miR-27a, and ECM-related molecules were also detected by quantitative real-time PCR (qPCR). We found that miR-27a inhibitor inactivated Wnt\/\u03b2-catenin signalling and reduced ECM deposition. Conversely, Wnt\/\u03b2-catenin signalling was activated, while ECM deposition was increased after transfection with si-Sfrp1. Interestingly, miR-27a inhibitor attenuated the effects of si-Sfrp1. We concluded that miR-27a down-regulated Sfrp1 and activated Wnt\/\u03b2-catenin signalling to promote renal fibrosis.<\/jats:p>","DOI":"10.1042\/bsr20192794","type":"journal-article","created":{"date-parts":[[2020,6,2]],"date-time":"2020-06-02T12:01:12Z","timestamp":1591099272000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["MicroRNA-27a targets Sfrp1 to induce renal fibrosis in diabetic nephropathy by activating Wnt\/\u03b2-Catenin signalling"],"prefix":"10.1042","volume":"40","author":[{"given":"MingJun","family":"Shi","sequence":"first","affiliation":[{"name":"State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PingPing","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ZhongQiang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YingYing","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"LingLing","family":"Qu","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"XingMei","family":"Liu","sequence":"additional","affiliation":[{"name":"Guizhou Provincial People\u2019s Hospital, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YuanYuan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"XingCheng","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China"},{"name":"Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, 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