To examine the role of CITED2 in myocardial ischemia/reperfusion injury (MIRI) in a cell model and uncover the mechanism, hypoxia/reoxygenation (H/R) -stimulated H9C2 cell model was utilized as a MIRI cell model. Quantitative polymerase chain reaction (qPCR) as well as immunoblot assays were carried out to determine the expression of CITED2 in the MIRI cell model. MTT as well as lactate dehydrogenase assays were employed to detect the survival of H/R-stimulated H9C2 cells. Immunoblot, flow cytometry, qPCR, and enzyme-linked immunosorbent assay were carried out to assess the pyroptosis and inflammation in H9C2 cells. Immunoblot assays were used to confirm the mechanism. The expression of CITED2 was low in H/R-stimulated H9C2 cells. CITED2 can increase the survival of H/R-stimulated H9C2 cells. Additionally, CITED2 restrained H/R-stimulated pyroptosis of H9C2 cells. It also restrained the release of H/R-induced inflammatory factors. Mechanically, CITED2 inhibited HIF-1α expression, thereby suppressing MIRI progression. CITED2 attenuates MIRI in cardiomyocytes via mediating HIF-1α expression.
Keywords: H9C2; HIF-1α; Inflammatory factors; Myocardial ischemia/reperfusion injury.