HAND2-AS1 associates with outcomes of acute coronary syndrome and regulates cell viability of vascular endothelial cells.

Abstract

Acute coronary syndrome (ACS) is an emergency and severe disorder of the cardiovascular system. This paper assessed the expression of plasma HAND2-AS1 in patients with ACS, researched its diagnostic and prognostic significance, and studied its possible mechanism for participating in ACS. The concentration of HAND2-AS1 of 101 included patients with ACS was certified by qRT-PCR and its possible diagnostic function was revealed by the receiver operating characteristic (ROC) curve. All patients were followed up for 6months after percutaneous coronary intervention (PCI) therapy and Kaplan-Meier (K-M) curve and COX regression analysis was performed to estimate the short-term prognostic value of HAND2-AS1 in ACS. The interrelationship between HAND2-AS1 and Gensini score and endothelial injury was identified via Pearson correlation. The function of HAND2-AS1 on the viability, migration, and apoptosis of human umbilical vein endothelial cells (HUVECs) was estimated by the Cell Counting Kit-8 (CCK-8), Transwell chamber, and flow cytometry. In ACS patients, the expression of serum HAND2-AS1 was prominently decreased and closely correlated with the Gensini score. The decreased HAND2-AS1 expression was of diagnostic significance. Declined plasma HAND2-AS1 was observed in patients with the major adverse cardio-cerebrovascular event (MACCE) and was an independent risk for the poor prognosis of ACS patients. In the cell model, upregulation of HAND2-AS1 improved cell viability and migration and inhibited cell apoptosis. HAND2-AS1 was an independent biomarker for the diagnosis and prognosis of ACS. HAND2-AS1 might be involved in ACS development by regulating endothelial damage.