Long Noncoding RNA HOTAIR Functions as a Competitive Endogenous RNA to Regulate Connexin43 Remodeling in Atrial Fibrillation by Sponging MicroRNA-613

Abstract EN

Several studies have indicated that long noncoding RNAs (lncRNAs)-HOX transcript antisense RNA (HOTAIR) is involved in some cardiovascular diseases by regulating gene expression as a competitive endogenous RNA (ceRNA).

GJA1 encoding Cx43 is one potential target gene of microRNA-613 (miR-613).

Meanwhile, there is a potential target regulatory relationship between HOTAIR and miR-613.

The present study is aimed at investigating whether HOTAIR functions as a ceRNA to regulate the Cx43 expression in atrial fibrillation (AF) by sponging miR-613.

The expressions of HOTAIR, miR-613, and Cx43 were detected in the right atrial appendages of 45 patients with heart valve disease, including 23 patients with chronic AF.

The HOTAIR overexpressed and underexpressed HL-1 cell model were constructed to confirm the effect of HOTAIR on Cx43.

Then, the Cx43 expression was detected to testify the interplay between HOTAIR and miR-613 after cotransfecting HOTAIR and miR-613.

Furthermore, luciferase assays were performed to verify that HOTAIR could regulate Cx43 remolding as a ceRNA by sponging miR-613.

The expression of HOTAIR and Cx43 was significantly downregulated in chronic AF group.

HOTAIR regulated positively the Cx43 expression in HL-1 cells.

The upregulated effect of HOTAIR on the Cx43 expression could be remarkably attenuated by miR-613.

Moreover, the inhibitory effect of miR-613 on the Cx43 expression could be obviously mitigated by HOTAIR.

At last, luciferase assays confirmed HOTAIR functioned as a ceRNA in the Cx43 expression by sponging miR-613.

Our study suggests that HOTAIR, functioning as a ceRNA by sponging miR-613, is an important contributor to Cx43 remolding in AF.