Hypertrophic scarring (HS) is a common skin disorder that occurs during the wound healing process, and the pathogenesis of HS remains unclear. Increasing evidence indicated that specific microRNAs (miRs) may be involved in the onset and progression of HS. In the present study, the association between miR-22 and HS was investigated. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to examine the expression of miR-22 in 30 HS and matched normal skin tissues. In addition, human hypertrophic scar fibroblasts (HSFBs) were cultured and transfected with miR-22 mimics, and MTT and Annexin V apoptosis assays were performed to investigate the role of miR-22 in the proliferation and apo... More
Hypertrophic scarring (HS) is a common skin disorder that occurs during the wound healing process, and the pathogenesis of HS remains unclear. Increasing evidence indicated that specific microRNAs (miRs) may be involved in the onset and progression of HS. In the present study, the association between miR-22 and HS was investigated. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to examine the expression of miR-22 in 30 HS and matched normal skin tissues. In addition, human hypertrophic scar fibroblasts (HSFBs) were cultured and transfected with miR-22 mimics, and MTT and Annexin V apoptosis assays were performed to investigate the role of miR-22 in the proliferation and apoptosis of the human HSFBs. Next, RT-qPCR and western blot assays were performed to compare the expression levels of mitogen-activated protein kinase kinase (MEK), extracellular signal-regulated kinase (ERK) and p21 in untransfected and miR-22 mimic-transfected skin fibroblasts. The results identified that miR-22 was significantly downregulated in HS tissues as compared with the normal skin. Furthermore, transfection with miR-22 mimics in human HSFBs led to inhibited cell proliferation, increased apoptosis, as well as to decreased MEK expression and ERK1/2 phosphorylation, and increased expression of p21. In conclusion, the present study was the first to prove that aberrant expression of miR-22 may serve an important role in the pathogenesis of HS by regulating the MEK/ERK/p21 pathway, thus suggesting that miR-22 has the potential to become a therapeutic target for the treatment of HS.
