Effect Of Lentivirus-Mediated Overexpression Of Dkk3 On Apoptosis Of Hypertrophic Scar Fibroblasts
Keywords
Dkk3 Gene^Hypertrophic Scar Fibroblasts^Apoptosis^Collagen^Cytochrome C
Abstract
Abstract Purpose: To explore the effect of lentivirus-mediated overexpression of DKK3 on the apoptosis of hypertrophic scar fibroblasts. Methods: Human hypertrophic scar fibroblasts were isolated and cultured in vitro, and the cells were divided into control group, negative control lentivirus infection (vector) group and pcDNA3.1-DKK3 lentivirus infection (DKK3) group, RT-qPCR and Western Blot was used to detect the overexpression effect, MTT was used to detect cell viability, flow cytometry was used to detect cell apoptosis, and Western blot was used to detect activated caspase-9 (cleaved caspase-9), type ¢ò collagen (COL II), and type ¢ñ collagen (COL) in cells. I) and activated caspase-3 (cleaved caspase-3) and changes in the expression of cytochrome C (cytochrome C) protein in the cytoplasm and mitochondria. Results: DKK3 mRNA and protein expression levels increased in hypertrophic scar fibroblasts after pcDNA3.1-DKK3 infection (P<0.05). The viability of hypertrophic scar fibroblasts in the DKK3 group decreased, the apoptosis rate increased, the protein levels of cleaved caspase-9 and cleaved caspase-3 increased, and the protein levels of COL II and COL I decreased. Compared with vector cells, the cytoplasmic The level of cytochrome C protein in mitochondria increased and the level of cytochrome C protein in mitochondria decreased (P<0.05). Conclusion: Lentivirus-mediated overexpression of DKK3 can induce apoptosis in hypertrophic scar fibroblasts and reduce collagen synthesis by the cells. Service Recommend this article to friends Add to my bookshelf Add to citation manager E-mail Alert RSS Author-related articles Ke Xiaoping Zhang Qiguo Lin Weijia Cai Liangqi Service Author-related articles For further information of this article and research, feel free to contact our team for asssitance. Original research was done by Zhang Qiguo, Lin Weijia, Ke Xiaoping, Cai Liangqi
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