MiR-564 promotes hypertrophic scar formation through TGF-β1 upregulation.

Abstract

To evaluate the role of microRNA564 (miR-564) in the development of hypertrophic scar and investigate the possible mechanism of this process. The hypertrophic scar (HS) tissues and adjacent normal skin (NS) tissues were selected from 10 patients. The fibrosis-related proteins were detected via hematoxylin eosin (HE) staining, Masson staining and immunohistochemical detection. The relative expression difference of miR-564 in NS tissues and HS tissues was detected via reverse transcription-polymerase chain reaction (RT-PCR). The protein expression difference of transforming growth factor-β1 (TGF-β1) in NS tissues and HS tissues was detected via Western blotting. Moreover, the hypertrophic scar fibroblast (HSF) cells were isolated from HS tissues and divided into four groups according to different treatment methods: blank control group, scramble-transfected negative control group, miR-564 inhibitor-transfected miR-564 inhibitor group, and miR-564 plasmid-transfected miR-564 mimic group. The expressions of TGF-β1 in blank control group, scramble group, miR-21 mimic group and miR-21 inhibitor group were detected via RT-PCR and Western blotting. MiR-564 was highly expressed in HSF cells. Compared with that of blank control group, the expression of TGF-β1 was down-regulated through inhibiting the miR-564 expression, thus inhibiting the activation and proliferation of HSF cells. However, the overexpression of miR-564 achieved the opposite results. Up-regulated mir-564 promoted the development of hypertrophic scar via enhancing the expression of TGF-β1. MiR-564 may be a potential novel molecular target for the treatment of hypertrophic scarring.