Hypoxia – as a Possible Regulator of the Activity of Epicardial Mesothelial Cells After Myocardial Infarction

Aim To study the effect of hypoxia on activity epithelial-mesenchymal transition (EMT) in epicardial cells, which provides formation a specialized microenvironment. Material and methods This used model experimental myocardial infarction created by ligation anterior descendent coronary artery. The cells after hypoxic exposure was studied with marker, pimonidazole, bromodeoxyuridine, immunofluorescent staining heart cryosections, vitro mesothelial cell culture. Results undamaged maintained quiescent condition low levels their proliferation, extracellular matrix protein production, EMT activity. Acute ischemic injury induced moderate epicardial/subepicardial region. caused global rearrangement this region due to initiation changes composition, accumulation proteins. We found that may result smooth muscle precursors, fibroblasts, population Sca-1+ cardiac progenitor both participate construction new blood vessels serve as mesenchymal link for paracrine support microenvironmental cells. In experiments, we showed 72‑h facilitated activation regulatory genes, dissembling intercellular contacts, uncoupling, increased plasticity. Conclusion epicardium an adult serves “reparative reserve” can be reactivated exposure. creates basis approach influence modulate its regulating reparative processes.