| Objective: Cardiovascular diseases has become the main cause of getting sick and death.Myocardial infarction can lead to functionnal lost of regional myocardial, then scarwhich is formation of fibrous tissue would repair the necrosis area, which will lead toirreversible changes of heart’s structure and function, further deterioration can lead tofunctional lost of heart and then cardiac death. Clinically for acute myocardial infarctionin the case of without considering the heart transplant through medication and surgerytherapy effect is not significant, only one year mortality still high. Whether there in theheart has stem cells with the ability of self-renewal and differentiation has been thefocus topic of the research these years. A large number of domestic and foreignresearches prove that human myocardial cells has the ability of self-renewal, but theclinical researches show that the self-renewal is not enough to effectively fill theinfarction area of myocardial cell necrosis and lost. Studies show that cardiac stemcells(CSCs) are more likely to exist in the atrium and apex region, according to thesurface antigen of CSCs classification, most stem cell express c-kit+type, it is a kind ofstem cell factor receptor c-kit positive myocardial precursor cells that can renew itself,colony-forming cell line and can differentiate into myocardial cells, smooth muscle cellsand endothelial cells of pluripotent stem cells, cell transplantation in mice experimentshave established that these cells can be formed in the infarction area differentiationincluding myocardial tissue myocardial cells, and capillaries. The migration of CSCs tothe pathological changes’ region and the differentiation to fill and repair necrotic tissueswill not be successfully done without the combination of a variety of cytokines.Insulin-like growth factor(IGF-1) plays an important role in promoting celldifferentiation and the wound healing of muscle and endothelial tissue. CSCs guide IGF1receptor and its signal pathways through paracrine role to promoting myocardial cell survival, and then enhance the CSCs autocrine role to enhance CSCs’ differentiationability in infarction myocardial tissue. Hepatocyte growth factor (HGF) can promote theproliferation and differentiation and migration of cells, its specific surface of membranereceptor express in a variety of tissue cells, including myocardial cells and vascularendothelial cells. In this experiment, by examining the CSCs in human myocardialtissue and the expression of its primary transcription factor cytokines of MEF-2C todemonstrate IGF1and HGF in CSCs relevant role in the process of differentiation,proliferation, thus providing a new method for clinical treatment of myocardialinfarction.Method: Study selects autopsy cases(total63cases) of year2011to2013from DalianMedical University clinical pathology center, including43cases which got myocardialinfraction within no more than one week alive,20cases of normal control group. Allautopsy cases have been identified through histology, each of which I selected apex,atrium, left ventricle anterior wall, wall after and each of them I take a piece of wax,using the continuous ultra-thin biopsy technique, then detect cytokines, HGF and IGF-1c-kit+CSCs myocardial primary transcription factor expression of MEF-2C in infarctarea and around the infarction area by using immunohistochemical S-P technique, thenanalysis of the correlation between the factors by statistics, from which we discusswhether the IGF-1, HGF have effect on promoting expression of c-kit+CSCs.Result: The expression positive rate of c-kit in the infarction area and around theinfarction area were75%and68%respectively, and mainly expressed in the myocardialcell membrane and cytoplasm, only5cases from normal control group expresspositively, the positive rate was25%, the chi-square test P<0.05, compared tomyocardial infarction area and the surrounding area, which show significant difference.IGF1in the infarction area and the surrounding area of positive rate were79%and75%respectively, compared with the normal control group expression rate of30%, whichalso has significant difference. HGF mainly express in cell membrane and cytoplasm,expression positive rate of which in infarction area and the surrounding area were68%and65%respectively, significant difference was found compare with normal tissues which was only20%. The expression positive rate of MEF-2C in the infarction area andthe surrounding area were77%and58%respectively, compared with normal myocardia-l expression positive rate which is20%, P<0.05shows these differences are significant.Through the Spearman correlation analysis IGF-1, HGF expression in the infarctionarea was associated with a c-kit expression significantly, P<0.01, the correlationcoefficient of which is0.539and0.616respectively.Conclusion:1. There is small amount of c-kit+CSCs in the normal myocardial tissue, while inmyocardial infarction lesions the degree of expression highly increased. After theoccurrence of myocardial infarction, the expression amount of transcription factorMEF-2C significantly increased,from which we suggest there has increasing number ofdifferentiation of CSCs.2. The IGF-1rarely expressed in normal myocardial tissue, while after theoccurrence of myocardial infarction, the expression quantity increased in the infarctionarea and the surrounding area, and it has quantity positively correlated with c-kitexpression, suggested its expression has a positive role in promoting, participate inpromoting the c-kit+CSCs mobilization and differentiation.3. HGF expression in normal tissue was less, but after infarction its expressionquantity increased in the infarction area and the surrounding tissue, and positivelycorrelated with increased the expression of c-kit, prompt it plays an important role the inthe differentiation of c-kit+CSCs. The promotion of c-kit+CSCs’s expression anddifferentiation function by IGF1and HGF is implemented through different pathways,and the synergy is less. |
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