F Liu1, W-W Chen, Y Li, J-Q Zhang, Q-B Zheng. 1. Department of Plastic Surgery, Affiliated Hospital of Jining Medical University, Jining, China. zhengqibingjn@sina.com.
Abstract
OBJECTIVE: To explore the role of micro ribonucleic acid (miR)-6836-3p in regulating hypertrophic scar (HS) and its potential mechanism. PATIENTS AND METHODS: The level of miR-6836-3p in HS or normal skin was determined by Real-Time Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Cell counting kit-8 (CCK8) and flow cytometry were applied to explore the effect of miR-98 on the growth and apoptosis of HS fibroblasts (HSFBs). Luciferase assay was employed to acknowledge whether connective tissue growth factor (CTGF) is a target of miR-6836-3p. Western blotting was used to detect the protein expression of CTGF after transfection with miR-6836-3p mimic or inhibitor. RESULTS: MiR-6836-3p expression was much higher in HS than that in normal skin. MiR-6836-3p mimic promoted fibroblast growth, and CTGF was confirmed to be a direct target of miR-6836-3p. The results of Western blotting clarified that miR-6836-3p mimic raised the level of CTGF, and its expression was positively correlated with that of CTGF. CONCLUSIONS: MiR-6836-3p promoted the development of HS by increasing the expression of CTGF. MiR-6836-3p may be a potential novel molecular target for the treatment of HS.
OBJECTIVE: To explore the role of micro ribonucleic acid (miR)-6836-3p in regulating hypertrophic scar (HS) and its potential mechanism. PATIENTS AND METHODS: The level of miR-6836-3p in HS or normal skin was determined by Real-Time Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Cell counting kit-8 (CCK8) and flow cytometry were applied to explore the effect of miR-98 on the growth and apoptosis of HS fibroblasts (HSFBs). Luciferase assay was employed to acknowledge whether connective tissue growth factor (CTGF) is a target of miR-6836-3p. Western blotting was used to detect the protein expression of CTGF after transfection with miR-6836-3p mimic or inhibitor. RESULTS: MiR-6836-3p expression was much higher in HS than that in normal skin. MiR-6836-3p mimic promoted fibroblast growth, and CTGF was confirmed to be a direct target of miR-6836-3p. The results of Western blotting clarified that miR-6836-3p mimic raised the level of CTGF, and its expression was positively correlated with that of CTGF. CONCLUSIONS: MiR-6836-3p promoted the development of HS by increasing the expression of CTGF. MiR-6836-3p may be a potential novel molecular target for the treatment of HS.