Myocardial infarction (MI) is a common cardiovascular disease characterized by an interruption of blood and oxygen supply to the heart, which results in gradual damage to the myocardial tissue and ultimately heart failure. The role of non-coding RNAs (lncRNAs) in the pathology of MI remains in its infancy, but has been implicated in MI and other heart conditions. For example, expression of a non-coding RNA hypoxia-inducible factor 1 alpha (HIF1A)-antisense RNA 2 (HIF1A-AS2) has previously been linked to coronary heart disease, however, whether HIF1A-AS2 expression is also high in MI has not been addressed. Here we reported that HIF1A-AS2 is upregulated in hypoxia-treated human cardiomyocytes (HMCs) compared with normal cardiomyocytes, and that silenced HIF1A-AS2 inhibited apoptosis and facilitated viability, migration and invasion of HMCs. Our data suggested that in MI, HIF1A-AS2 upregulation was associated with miR-623, which promoted expression of TRIM44. Moreover, by upregulating TRIM44 we were able to remedy the HIF1A-AS2 repression of apoptosis in HMCs. Thus we concluded that cardiomyocytes can be protected against hypoxic-treated injury by knockdown of HIF1A-AS2, which suppresses TRIM44, and that HIF1A-AS2 overexpression is a prognostic indicator of MI. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.