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HOTAIR promotes inflammatory response after acute myocardium infarction by upregulating RAGE.

OBJECTIVE
The aim of this study was to explore the role of HOTAIR in inflammatory response after acute myocardium infarction (AMI) and to investigate its underlying mechanism.


MATERIALS AND METHODS
The AMI model was first constructed in rats, and heart tissues were harvested. Expression levels of HOTAIR and receptor of advanced glycation end-products (RAGE) in rat heart were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The protein expression level of pEKR in rat heart was detected by Western blot. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in rats were determined by enzyme-linked immunosorbent assay (ELISA). The hypoxia-induced H9C2 cells were used to construct the MI model in vitro. Meanwhile, the expression levels of HOTAIR and RAGE in H9C2 cells were detected. The levels of TNF-α and IL-6 in the culture medium were determined by ELISA. Rescue experiments were conducted by co-transfecting pcDNA-HOTAIR and si-RAGE in H9C2 cells. Subsequently, the levels of pERK, TNF-α, and IL-6 were detected.


RESULTS
The mRNA expression levels of HOTAIR and RAGE in the AMI group were significantly higher than those of the control group. Western blot showed remarkably higher protein levels of RAGE and pERK in AMI rats when compared with those of controls. Similarly, results of ELISA indicated that the levels of TNF-α and IL-6 in AMI rats were significantly higher than those of controls. Meanwhile, overexpression of HOTAIR in H9C2 cells remarkably elevated the expression levels of HOTAIR and RAGE. In addition, upregulated pERK, TNF-α, and IL-6 were observed in H9C2 cells overexpressing HOTAIR, which could be reversed by RAGE knockdown.


CONCLUSIONS
HOTAIR promotes inflammatory response after AMI by upregulating RAGE expression.