LncRNA 1700020I14Rik/miR-297a/CGRP axis suppresses myocardial cell apoptosis in myocardial ischemia-reperfusion injury

Background: Long non-coding RNAs (lncRNAs) are closely related to various human diseases, but their role in myocardial injury has not been fully elucidated. In the current study, we found that the expression of lncRNA 1700020I14Rik was significantly down-regulated in myocardial injury tissues and the underlying mechanism by which lncRNA 1700020I14Rik regulated myocardial cell injury was investigated. Methods: The model of myocardial ischemia-reperfusion (I/R) injury and myocardial cells hypoxia/reoxygenation (H/R) injury were established and the expression of 1700020I14Rik, miR-297a or CGRP was analyzed by qRT-PCR or Western blot. Moreover, myocardial cell apoptosis was assessed by TUNEL staining and the concentration of LDH in the mouse plasma sample or myocardial cell culture supernatant was measured by the LDH cytotoxicity test kit. Furthermore, the differences of myocardial cell survival rate after H/R treatment were assessed by MTT assay and the observation of CGRP expression was performed in HL-1 cells overexpressed or silenced with 1700020I14Rik or miR-297a. In addition, the regulating function of miR-297a on 1700020I14Rik and CGRP expression was analyzed by a dual luciferase reporter assay. Results: The expressions of 1700020I14Rik and CGRP were abnormally down-regulated in a model of myocardial I/R injury and myocardial cells H/R injury, while miR-297a was up-regulated. By TUNEL staining, the apoptotic rate of myocardial cells in the model of myocardial I/R injury was significantly increased. Furthermore, the concentrations of LDH in the mouse plasma sample or myocardial cell culture supernatant were significantly increased after myocardial cell injury. By MTT assay, the survival rate of cells was decreased after myocardial cells were treated with H/R. In addition, overexpression of 1700020I14Rik or knockdown of miR297a could up-regulate CGRP protein level, while interference with 1700020I14Rik or overexpression of miR297a produced the opposite result. Further study confirmed that lncRNA 1700020I14Rik/miR-297a/CGRP axis suppressed myocardial cell apoptosis in myocardial I/R injury. Conclusion: Our results indicated that 1700020I14Rik was abnormally down-regulated in myocardial injury tissues. In-depth studies manifested that 1700020I14Rik/miR-297a/CGRP axis suppressed myocardial cell apoptosis in myocardial I/R injury.