Effect Of SCD1 Overexpression On The Endothelial Differentiation Of Bone Marrow Mesenchymal Stem Cells

Objective: Explored the effect of Stearoyl-Co A desaturase 1(SCD1)overexpression on the endothelial differentiation function of human bone marrow mesenchymal stem cells(BM-MSCs)and genes expression profile,through the gene chip and intelligent pathway analysis system(IPA).Explore the mechanism how SCD1 effects the endothelial differentiation of BM-MSCs.Methods: Used the SCD1 lentivirus which had been successfully built to transfect BM-MSCs.Performed RT-PCR to detect the expression of SCD1 and used ratio of([14C] oleic acid)/([14C] oleic and stearic acids)to detected the activity of SCD1.After endothelial induction culture,used RT-PCR,immunofluorescence and Western blot technique to detect the endothelial index including CD31,v WF and CDH5.Gene microarray was performed and used the Ingenuity Pathway Analysis(IPA)system to analyze the differential gene expression profile of the BM-MSCs modulated by SCD1 overexpression.Results: SCD1 was stably overexpressed in BM-MSCs and maintained a highly activity.RT-PCR results showed that compared with the control group,the endothelial markers CD31,v WF and CDH m RNA in the overexpressed group were higher than those of the control group(p<0.05).The results of cell immunofluorescence and WB showed that the expression of endothelial index in overexpressed group was significantly higher.The microarray showed there are total 522 differential expression genes.The results of flow cytometry showed that the level of ROS in the overexpressed group was significantly lower and the S stage cells were more than the control group.Conclusion: SCD1 expression can promote the endothelial differentiation of BM-MSCs by reducing the cell oxidative stress and improving the ability of cell proliferation differentiation.The role of SCD1 in promoting the endothelial differentiation of BM-MSCs may provide a new strategy for endothelial function repair,cardiovascular disease treatment and vitro osteogenesis.