ABSTRACT
Cardiomyocytes are highly differentiated terminal cells with poor self-renewal ability. Therefore, after myocardial infarction necrotic cardiomyocytes cannot be effectively replenished, and the infarcted area is quickly replaced by fibrous tissue, which seriously affects cardiac function. The reduction of the number of myocardial cells and the destruction of the structural integrity of the heart have caused cardiovascular diseases such as myocardial infarction and heart failure, which continue to endanger human life and health. At present, the treatment of coronary heart disease has made great progress. The commonly used treatment options for myocardial repair after myocardial infarction mainly include stem cell transplantation, exosome mediation and microenvironment construction, but all of them are difficult to solve to varying degrees. Cardiac fibroblasts occupy the majority of cardiac cells, and the distribution characteristics of fibroblasts and their role in the process of myocardial infarction make them important effector cells after myocardial infarction. Therefore, this article reviews the source, distribution, post-infarction status of myocardial fibroblasts and the effect of fibroblasts on cardiomyocytes, in order to provide new treatment ideas and solutions for fibroblasts in the repair and regeneration of myocardial cells after myocardial infarction.
ABSTRACT
Aim To explore the pro-angiogenesis effect of exosomes derived from human umbilical cord mesenchymal stem cells on cardiac myofibroblasts. Methods The surface markers of hucMSC were detected by flow cytometry. Exosomes were identified by transmission electron microscopy, Nanosight nanoparticle analyzer and Western blot. The effects of exosomes treated cardiac myofibroblasts on endothelial cell proliferation, migration and tubule formation were detected by CCK-8 cell proliferation assay, Transwell assay, cell scratching and endothelial tubule formation assay. The levels of VEGF-A in cardiac myofibroblasts in the control and exosomes-treated group were detected by real-time quantitative PCR etc. After β-catenin/ TCF-mediated transcription inhibitors were added, the expression levels of VEGF-A were detected by Western blot. Results hucMSC did not express CD19, CD34 and CD45, but expressed CD29, CD105 and CD90, which was consistent with the characteristics of mesenchymal stem cells. Exosomes were identified with a particle size of about 100 -200 nm. Compared with hucMSC, exosomes expressed high CD81, low GAPDH, and no Calnexin. Immunofluorescence cytochemical staining revealed that cardiac myofibroblasts expressed α-SMA, and exosomes treated cardiac myofibroblasts promoted endothelial cell proliferation, migration and tubule formation. Further detection showed that the level of VEGF-A in cardiac myofibroblasts increased after exosomes treatment, and the expression level of VEGF-A decreased after β-catenin/ TCF-mediated transcription inhibitor was used. Conclusions Exosomes derived from hucMSC enhance the angiogenesis of cardiac myofibroblasts.