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Objective: To provide different sources of differentiated cells to myocardial injury site , can promote myocardial and microvascular regeneration and improve heart function . Study found that cardiac progenitor cells (CPCs) has a strong self-renewal , colony formation and differentiation potential , easy to produce effective electrical coupling is more suitable than other sources of cells used to repair myocardial infarction organization , but the cells in the ischemic hypoxia and inflammation infarction environment in the utilization rate is very low . Trop2 is an expression at the cell surface glycoprotein , can enhance a variety of cell viability , but no studies to confirm the role of the CPCs . This study was designed to observe the the Trop2 CPCs can improve the anti-apoptotic ability to improve the utilization of the CPCs the treatment of myocardial infarction . Method : c-kit cells frozen recovery after passage divided into three groups : c -kit cells transfected Trop2 genomic c -kit cells to silence Trop2 gene group , c-kit cells group . Were treated with H2O2 (0,30,60,120 μmol / L train 1h ) hypoxia (0,5 % , 10% , 21% O2 for 48h) and LPS ( lipopolysaccharide 0,10,100,1000 ng / ml cultured for 24 hours ) stimulation. Flow cytometry AnnexinV / PI double staining rate of apoptosis. Western-blot to detect the expression of PKCα in Raf- 1 , Bcl -2 , Bax expression level of PKCα in Raf- 1 phosphorylation levels . The experiments were repeated three times . Results : Trop2 of gene mouse cardiac c-kit cells can promote the anti-apoptotic . Flow cytometry Annexin V / PI double staining apoptosis rate found in the the H2O2, hypoxic and LPS stimulation , Trop2 apoptosis of expression group were lower than the control group , and / or silent group . Western-blot detected Trop2 overexpression group compared to the other two groups , Bcl-2 expression levels of PKCα in Raf- 1 phosphorylation levels raised , Bax was down . Conclusion : Trop2 has the ability to promote the anti-apoptotic c-kit cells in simulated myocardial infarction microenvironment . The mechanism may be through Trop2 activation , activate PKCα, phosphorylation more Trop2 , form a positive feedback . Further up-regulates Bcl-2 and downregulation of Bax expression levels , start the mitochondrial apoptotic pathway , and the phosphorylation of Raf - 1 through the Ras / Raf / MEK / ERK pathway , play an anti-apoptotic effects . Trop2 ligand has not yet been discovered , so Trop2 specific activation mechanism still needs further study .
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