MECHANISM OF CONJUGATION OF THE FUNCTIONS OF CARDIAL AND MESENCHEME STEM CELLS IN THE MYOCARDIUM

Abstract

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RELEVANCE. The mechanisms of interaction of resident cardiac and mesenchymal stem cells of the bone marrow (KSK, MSCCM) in tissues remain largely unclear. PURPOSE. To evaluate the role of apoptotic bodies of cardiomyocytes (AptK) and fibroblasts (AptF) in conjugation of functions of KSK and MSCCM. Materials and methods. Influence of ApT on cardiomyogenesis was studied in the model of cardiomyogenesis from KSK (c-kit + , Sca + , Isl1 +). Myocardial infarction (MI) caused in Wistar and Wistar-Kayoto rats. Emigration of MSCCM to the myocardium after MI was studied by in situ hybridization on the Y chromosome. The directional migration of the MFCI with the GFP tag was studied in C57BL / 6 mice. Cell preparations and tissue sections were examined by confocal microscopy. Myocardial contractility was evaluated ex vivo by Langendorf. RESULTS. It was shown that the co-cultivation of myocardium and apTK cells accelerated the proliferation and differentiation of CCC in the colony. The frequency of reduction of colonies after 3 weeks of co-cultivation increased in comparison with the control by more than 1.5 times. ApTF had no effect on cardiomyogenesis. After the administration of ApTK to rats with postinfarction heart failure, the contractility of the ventricle was increased by 30% 3 weeks after the infarction. Injections of ApTK into the "old” rats caused an increase in myocardial contractility to values characteristic of the heart of "young” animals. ApTF inhibited contractility of the myocardium. It was shown that ApTK was activated in the myocardium by the restoration of a pool of cardiomyocytes (c-kit +, a-Actinin), and АТТF stimulated the development of clones from which the endothelium is formed (Sca+, CD 105). It is shown that the MSCMM of males injected into females after MI was detected in the perifocal zone of damage outside the vessels and in the wall of newly formed vessels. In ex vivo experiments, laser doses were identified that caused predominantly apoptosis (I) or necrosis of cells (II). It was shown that after irradiation of (I) tissues and administration of MSCKM with GFP in a day, mesenchymal cells accumulated in the laser exposure zone. With the use of (II), the transfer of MQCM from the bloodstream to the tissue was not observed. CONCLUSIONS. It seems that the functions of KSK and MSCCM in the zones of myocardial regeneration are interfaced by means of ATp cells. On the surface of ATp there are signal molecules that determine the directed movement of MSCCM into the zone of apoptosis, and inside АТp there are biologically active compounds that carry the tissue-specificity code of the dead cell.