Retracted: Intermedin attenuates cardiomyocytes hypoxia‐injury through upregulating long noncoding RNA MALAT1

Abstract

Myocardial infarction (MI) is a life-threatening cardiovascular disease, and the prognosis is far from satisfied. It is reported that the protective role of intermedin (IMD), a bioactive peptide, in cardiomyocytes. Nevertheless, its mechanism remains unclear. In vitro hypoxia cell model was established according to the alteration of cell survival. Cell counting kit-8, Western blot, and flow cytometry assay were used to test cell viability, proliferation and apoptosis. Then, the toxicity of IMD was analyzed, the functions of IMD on hypoxia-injury were explored. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was utilized for measurements of metastasisassociated lung adenocarcinoma transcript 1 (MALAT1) expression in cells under hypoxia with or without IMD pretreatment. Whether IMD affected H9c2 cells through regulating MALAT1 was studied, and the possible involved signaling pathways were investigated. We found that hypoxiacaused decline of proliferation and the rise of apoptosis were remitted by IMD pretreatment. Hypoxia enhanced MALAT1 expression. MALAT1 expression was upregulated by IMD pretreatment. It was proved that functions of IMD pretreatment in hypoxia-induced H9c2 cells could be reversed by MALAT1 inhibition. Western blot analysis investigated IMD pretreatment elevated phosphorylated levels of phosphatidylinositol-3kinase (PI3K) and AKT as well as β-catenin levels through upregulating MALAT1. It was the first time found that IMD pretreatment could effectively remit H9c2 cell hypoxia-caused injury via the upregulation of MALAT1and PI3K/AKT and β-catenin pathways.