LncRNA-CARl in a rat model of myocardial infarction.

OBJECTIVE: To investigate how long non-coding ribonucleic acid-cardiac apoptosis-related (lncRNA-CARL) regulates apoptosis of primary endothelial cells. The specific role of lncRNA-CARL in the occurrence and development of myocardial infarction (MI) and atherosclerosis is also explored.

MATERIALS AND METHODS: A rat model of arteriosclerosis was prepared by extracting myocardial endothelial cells of rats. After the overexpression or inhibition of lncRNA-CARL, cell counting kit-8 (CCK-8) assay was used to detect cell activity. LncRNA-CARL plasmids were constructed and injected into the carotid artery in rats, and hematoxylin and eosin staining (HE) was used to observe the neointima of the carotid artery in rats. The activity of apoptosis protein Caspase-3 in endothelial cells was detected by Caspase-3 activity assay kit. Expressions of prohibitin-2 (PHB2), B-cell lymphoma-2 (Bcl-2) and Bcl-2-Associated X (Bax) protein were gauged by Western blot.

RESULTS: The over-expression of lncRNA-CARL in primary endothelial cells in rats could increase cell viability. LncRNA-CARL also down-regulated the expressions of PHB2 and Bax, reduced the activity of Caspase-3 and increased the expression of anti-apoptotic protein Bcl-2. LncRNA-CARL inhibition could significantly increase Caspase-3 activity and Bax expression, whereas decrease Bcl-2 expression (p<0.05). Local silencing of lncRNA-CARL in rats resulted in decreased intravascular intima-media thickness ratio and Bcl-2 expression, as well as increased activity of Caspase-3 and Bax expression (p<0.05).

CONCLUSIONS: Long non-coding ribonucleic acid-cardiac apoptosis-related lncRNA (lncRNA-CARL) regulates cell apoptosis and participates in the occurrence and development of MI.