Effect of mir-210-3p on The Function of c-kit+ Cardiac Progenitor Cells under Ischemia and Hypoxia

C-kit+ cardiac progenitor cells (CPCs) play an important role in improving the prognosis of ischemic heart disease. MicroRNAs have been shown to have a protective role in the cardiac repair process, but their specific functional mechanisms are still unclear. The aim of this study was to screen for differentially expressed miRNAs in c-kit+ CPCs under hypoxia and explore their effects on the function of c-kit+ CPCs. We found that miR-210-3p was significantly upregulated in hypoxia-treated c-kit+ CPCs through second-generation sequencing. Protein chip detection revealed that c-kit+ CPCs could express cytokines such as FGF basic, Angiogenin, and VEGF, and that hypoxia could enhance the secretion of some angiogenesis-related factors. Silencing miR-210-3p, on the other hand, resulted in a reduction in the secretion of these angiogenesis-related factors. In addition, we found that the conditioned medium of hypoxia-treated c-kit+ CPCs could promote the proliferation, migration, and tube formation ability of mouse cardiac microvascular endothelial cells (CMECs). Conversely, the conditioned medium of c-kit+ CPCs with silenced miR-210-3p after hypoxia inhibited the proliferation, migration, and tube formation ability of CMECs. These results suggest that c-kit+ CPCs may exert their pro-angiogenic effects through paracrine mechanisms, which are regulated by miR-210-3p. The upregulation of miR-210-3p in hypoxia-treated c-kit+ CPCs may enhance their paracrine function by regulating the secretion of angiogenic factors, thereby promoting angiogenesis in ischemic heart disease. Therefore, miR-210-3p plays a key role in regulating the paracrine function of c-kit+ CPCs and can affect the process of angiogenesis. The role of miR-210-3p has potential application value for the treatment of ischemic heart disease, and may become one of the important targets for future treatment of ischemic heart disease. Overall design: Take healthy adult male C57BL/6 mice aged 4-6 weeks, digest their hearts using trypsin and collagenase, and use anti-c-kit-coupled magnetic beads for magnetic-activated cell sorting (MACS) to isolate c-kit cells. Culture the cells under hypoxia for 12 hours to establish the hypoxia model. Randomly divide the cultured cells into a normal control group and a hypoxia group, and extract cellular RNA for miRNA sequencing.