LncRNA-P21 suppresses apoptosis of myocardial cells in rats with acute myocardial infarction via regulating Wnt/ß-catenin signaling pathway.

ABSTRACT

OBJECTIVE: The aim of this study was to investigate the expression of long non-coding ribonucleic acid (lncRNA)-p21 in rats with acute myocardial infarction (AMI) and its influences on the viability and apoptosis of myocardial cells. MATERIALS AND METHODS: Sprague-Dawley rats were utilized to establish the AMI model. Myocardial tissues were extracted, and myocardial cells were isolated. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of lncRNA-p21. Subsequently, myocardial cells of AMI rats were cultured and transfected with lncRNA-p21 or small interfering (si)-lncRNA-p21. 48 h later, cell proliferation was determined using Cell Counting Kit-8 (CCK-8). Caspase-3 kit was applied to examine the changes in Caspase-3 after myocardial cell transfection. Moreover, Western blotting assay was performed to measure the protein expressions of apoptosis-associated indexes [B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax)] and key members of the Wnt signaling pathway (Wnt-5a and ß-catenin). RESULTS: The expression of lncRNA-p21 decreased significantly in myocardial tissues (p<0.01). However, the mRNA expression of inflammatory factors was significantly upregulated in AMI group compared with those in Sham group (p<0.01). Compared with Vehicle group, LncRNA-p21 group exhibited remarkably enhanced myocardial cell viability (p<0.05). However, Si-lncRNA-p21 group weakened myocardial cell viability (p<0.05). The expression of Caspase-3 in myocardial cells was reduced in LncRNA-p21 group (p<0.05), but remarkably rose in Si-lncRNA-p21 group (p<0.05) in comparison with Vehicle group. In addition, the protein expressions of Wnt-5a and ß-catenin in myocardial cells were significantly higher in LncRNA-p21 group (p<0.05), whereas were lower in Si-lncRNA-p21 group (p<0.05) than those in Vehicle group. CONCLUSIONS: LncRNA-p21 was lowly expressed in myocardial tissues of AMI rats. Furthermore, it affected the proliferation, apoptosis and inflammation level of myocardial cells in AMI rats by activating the Wnt/ß-catenin signaling pathway.