LncRNA MALAT1 functions as a biomarker of no-reflow phenomenon in ST-segment elevation myocardial infarction patients receiving primary percutaneous coronary intervention

Abstract

AbstractMALAT1 was reported to sponge miR-30e, miR-126 and miR-155 in the pathogenesis of many diseases. Plasma miR-30e can indicate the risk of no-reflow during primary percutaneous coronary intervention (pPCI), while miR-126 can be used as a predictor of coronary slow flow phenomenon. In this study, we compared the diagnostic value of above genes in the prediction of no-reflow phenomenon in ST-segment elevation myocardial infarction (STEMI) subjects receiving pPCI. Quantitative real-time PCR, ELISA, Western blot and luciferase assays were performed to explore the regulatory relationship of MALAT1/miR-30e, MALAT1/miR-126, MALAT1/miR-155, miR-126/HPSE, and miR-155/EDN1. ROC analysis was carried out to evaluate the potential value of MALAT1, miRNAs and target genes in differentiating normal reflow and no-reflow in STEMI patients receiving pPCI. Elevated MALAT1, CRP, HPSE, and EDN1 expression and suppressed miR-30e, miR-155 and miR-126 expression was found in the plasma of STEMI patients receiving pPCI who were diagnosed with no-reflow phenomenon. ROC analysis showed that the expression of MALAT1, miR-30e, miR-126 and CRP could be used as predictive biomarkers to differentiate normal reflow and no-reflow in STEMI patients receiving pPCI. MALAT1 was found to suppress the expression of miR-30e, miR-126 and miR-155, and HPSE and EDN1 were respectively targeted by miR-126 and miR-155. This study demonstrated that MALAT1 could respectively sponge the expression of miR-30e, miR-126 and miR-155. And miR-30e, miR-126 and miR-155 respectively targeted CRP, HPSE and EDN1 negatively. Moreover, MALAT1 could function as an effective biomarker of no-reflow phenomenon in STEMI patients receiving pPCI.