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The mammalian cleavage factor I 25-kD subunit (CFIm25; encoded by NUDT21) is a key regulator of alternative polyadenylation, and its depletion causes predominantly 3\u2032UTR shortening through loss of stimulation of distal polyadenylation sites. A shortened 3\u2032UTR will often lack microRNA target sites, resulting in increased mRNA translation due to evasion of microRNA-mediated repression. Herein, we report that CFlm25 is downregulated in SSc skin, primary dermal fibroblasts, and two murine models of dermal fibrosis. Knockdown of CFIm25 in normal skin fibroblasts is sufficient to promote the 3\u2032UTR shortening of key TGF\u03b2-regulated fibrotic genes and enhance their protein expression. Moreover, several of these fibrotic transcripts show 3\u2032UTR shortening in SSc skin. Finally, mice with CFIm25 deletion in fibroblasts show exaggerated skin fibrosis upon bleomycin treatment, and CFIm25 restoration attenuates bleomycin-induced skin fibrosis. Overall, our data link this novel RNA-processing mechanism to dermal fibrosis and SSc pathogenesis.<\/jats:p>","DOI":"10.1084\/jem.20181384","type":"journal-article","created":{"date-parts":[[2019,11,22]],"date-time":"2019-11-22T19:45:13Z","timestamp":1574451913000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":44,"title":["Downregulation of CFIm25 amplifies dermal fibrosis through alternative polyadenylation"],"prefix":"10.1084","volume":"217","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6041-4788","authenticated-orcid":true,"given":"Tingting","family":"Weng","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, the University of Texas Health Science Center at Houston, Houston, TX 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingjing","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, the 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