MicroRNA-18a-5p represses scar fibroblast proliferation and extracellular matrix deposition through regulating Smad2 expression

xlomafota13 shared this article with you from Inoreader MicroRNA-18a-5p represses scar fibroblast proliferation and extracellular matrix deposition through regulating Smad2 expression Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1318. doi: 10.3892/etm.2021.10753. Epub 2021 Sep 20. ABSTRACT The aim of the present study was to investigate the expression and role of microRNA-18a-5p (miR-18a-5p) during the formation of hypertrophic scar (HS), and to further explore the molecular mechanisms involved. Downregulation of miR-18a-5p in HS tissues and human HS fibroblasts (hHSFs) was detected by reverse transcription-quantitative polymerase chain reaction. The binding sites between miR-18a-5p and the 3'-untranslated region of SMAD family member 2 (Smad2) were predicted by TargetScan and confirmed by dual-luciferase reporter assay. To investigate the role of miR-18a-5p in HS formation, the effects of miR-18a-5p downregulation or upregulation on hHSFs were subsequently determined. Cell proliferation was detected by an MTT assay, while cell apoptosis was measured by flow cytometry. In addition, the protein expression levels of Smad2, Collagen I (Col I) and Col III were examined by western blot assay. The findings indicated that miR-18a-5p downregulation in hHSFs significantly promoted the cell proliferation, decreased cell apoptosis and enhanced the expression levels of Smad2, Col I and Col III protein and mRNA, whereas miR-18a-5p upregulation in hHSFs exerted opposite effects. Notably, the effects of miR-18a-5p upregulation on hHSFs were eliminated by Smad2 upregulation. In conclusion, the data indicated that miR-18a-5p was downregulated during HS formation, and its upregulation repressed scar fibroblast proliferation and extracellular matrix deposition by targeting Smad2. Therefore, miR-18a-5p may serve as a novel therapeutic target for the treatment of HS. PMID:3463 0672 | PMC:PMC8495553 | DOI:10.3892/etm.2021.10753 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.