The current study aimed to explore the role and mechanism of microRNA-425-5p (miR-425-5p) in hypertrophic scar (HS) development. Firstly, we used reverse transcription-quantitative polymerase chain reaction (qRT-PCR)to detect the expression of miR-425-5p in human hypertrophic scar fibroblasts
(hHSFs) and HS tissues. qRT-PCR assay showed that miR-425-5p level significantly down-regulated in HS tissues and hHSFs. Next, we performed TargetScan and dual-luciferase reporter assay to predict and verify Smad2 was the target gene of miR-425-5p. In order to determine the role of miR-425-5p
in HS formation, miR-425-5p was over-expressed or knockdown in hHSFs through transfection with miR-425-5p mimic or miR-425-5p inhibitor. CCK-8 assay and cell apoptosis analysis were carried out to measure cell viability and apoptosis. Protein expression was assessed by Western blotting. The
findings indicated that miR-425-5p mimic transfection inhibited cell viability, promoted cell apoptosis and repressed Smad2, Col I, and Col III expression in hHSFs. Notably, the transfection of Smad2-plasmid eliminated the effects of miR-425-5p mimic on hHSFs. However, miR-425-5p inhibitor
transfection had opposite effects on hHSFs, and were eliminated by the transfection of Smad2-siRNA. In conclusion, these findings suggested that miR-425-5p inhibited the hHSFs viability, induced hHSFs apoptosis and repressed extracellular matrix deposition of hHSFs through regulating Smad2.
Therefore, miR-425-5p might be a novel therapeutic target for HS treatment.
Silencing of long noncoding INHBA antisense RNA1 suppresses proliferation, migration, and extracellular matrix deposition in human hypertrophic scar fibroblasts via regulating microRNA-141-3p/myeloid cell leukemia 1 axis
