{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,21]],"date-time":"2026-06-21T04:25:33Z","timestamp":1782015933739,"version":"3.54.5"},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2021,4,5]],"date-time":"2021-04-05T00:00:00Z","timestamp":1617580800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Wound Repair Regeneration"],"published-print":{"date-parts":[[2021,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hypertrophic scars (HSs) form due to unchecked proliferation of fibrous tissue after an injury to the skin. Recently, lncRNA MIR503HG was shown to be involved in HS. However, the mechanism by which MIR503HG affects the formation and progression of HS still needs further study. qRT\u2010PCR was applied to examine the levels of MIR503HG and miR\u2010143\u20103p in HS tissues and human hypertrophic scar fibroblasts (hHSFs). The relationships of MIR503HG, miR\u2010143\u20103p and Smad3 were explored with a dual\u2010luciferase reporter assay. Cell proliferation, apoptosis, and invasion were measured by CCK\u20108 assay, flow cytometry and transwell assay, respectively. The protein level of Smad3 was tested via Western blotting. MIR503HG was upregulated and miR\u2010143\u20103p was downregulated in HS versus normal skin tissues. The knockdown of MIR503HG and the overexpression of miR\u2010143\u20103p suppressed the proliferation and invasion of hHSF, and promoted cell apoptosis. MIR503HG bound to miR\u2010143\u20103p while miR\u2010143\u20103p directly targeted Smad3 to inhibit its expression. Suppression of miR\u2010143\u20103p and overexpression of Smad3, respectively, reversed these effects of knockdown of MIR503HG and overexpression of miR\u2010143\u20103p on hHSFs. Our research supports a model in which the MIR503HG\/miR\u2010143\u20103p\/Smad3 axis serves as a critical regulator of HS, highlighting a promising therapeutic option for HS.<\/jats:p>","DOI":"10.1111\/wrr.12913","type":"journal-article","created":{"date-parts":[[2021,4,5]],"date-time":"2021-04-05T18:28:58Z","timestamp":1617647338000},"page":"792-800","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["<scp>LncRNA MIR503HG<\/scp> promotes hypertrophic scar progression via <scp>miR<\/scp>\u2010143\u20103p\u2010mediated Smad3 expression"],"prefix":"10.1111","volume":"29","author":[{"given":"Jun","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Plastic and Burn Surgery the First Affiliated Hospital of Guangxi Medical University  Nanning Guangxi Zhuang Autonomous Region 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