MicroRNA26a inhibits hyperplastic scar formation by targeting Smad2

Abstract

Objective To investigate the expression of microRNA-26a (mir-26a) and its target gene mothers against decapentaplegic homolog 2 (Smad2) in hypertrophic scar (HS) and explore their possible roles in HS formation. Methods Twenty patients (including 13 female and 7 male patients aged 17~58 years) previously receiving scar excision and autologous skin grafting were enrolled in this study. Real-time qPCR and Western blotting were performed for detecting the expression of miR-26a and Smad2 in the HS tissues and paired normal skin (NS) tissues obtained from the patients and in human skin fibroblasts (CCC-ESF-1) and HS fibroblasts (hHSFs). A dual luciferase reporting system was used to verify whether Smad2 was the target gene of miR-26a. The changes in Col Ⅰ and Col Ⅲ in hHSFs in response to over-expression and interference of Smad2 were examined using RT-qPCR and Western blotting. Results The expression level of miR-26a was significantly lower and that of Smad2 was significantly higher in HS tissues and hHSF than in NS tissues (P < 0.05). Dual luciferase assay confirmed that miR-26a could target Smad2 to regulate the activity of the latter. Smad2 overexpression and knockdown obviously promoted and inhibited, respectively, the expression of Col Ⅰ and Col Ⅲ in hHSFs. Conclusion A low expression of miR-26a may contribute to the formation of HS by up-regulating its target gene Smad2.

Keywords

• microrna-26a
• target gene
• smad2
• hypertrophic scar