Interfering with STX18-AS1 protects cardiomyocytes by targeting miR-204

  AIM   To investigate whether interfering with LncRNA STX18-AS1 can up-regulate the expression of miR-204 to affect the myocardial cell hypoxia injury.

  METHODS   The cardiomyocytes H9C2 were cultured in vitro and the cardiomyocytes were treated with CoCl₂ to establish a model of cell hypoxia injury. The expression levels of STX18-AS1 and miR-204 at different time points of CoCl₂ treatment were detected by qRT-PCR. The experiment set up control group, model group, si-NC group, si-STX18-AS1 group, miR-NC group and miR-204 group. MTT was used to detect cell proliferation activity and flow cytometry and TUNEL were used to detect the apoptosis rate. The LDH activity, MDA level, SOD activity and CAT activity were detected using a biochemical kit and the targeting relationship of STX18-AS1 and miR-204 was verified by the dual luciferase report experiment.

  RESULTS   Compared with those in control group, the expression level of STX18-AS1 in model group and si-NC group was increased (P<0.01) and the expression level of miR-204 was decreased (P<0.01) at 6 h, 12 h, 18 h and 24 h treated with CoCl₂. Compared with those in si-NC group and si-NC group, the expression level of STX18-AS1 in si-STX18-AS1 group decreased (P<0.01) and the expression level of miR-204 increased (P<0.01) at 6 h, 12 h, 18 h and 24 h treated with CoCl₂. Compared with those in control group, the cell proliferation activity in model group and si-NC group decreased (P<0.01), apoptosis rate, LDH activity and MDA level were significantly increased (P<0.01) and the activity of SOD and CAT were significantly decreased (P<0.01). Compared with those in model group and si-NC group, the cell proliferation activity was significantly increased (P<0.01), cell apoptosis rate and the LDH activity and MDA level were notably reduced (P<0.01) and the activity of SOD and CAT were significantly increased (P<0.01). The effect of transfection of miR-204 mimics on the proliferation activity, apoptosis and oxidative stress of cardiomyocytes was the same as the effect of transfection of si-STX18-AS1. The dual luciferase report experiment confirmed that STX18-AS1 could target miR-204.

  CONCLUSION   Interfering with STX18-AS1 expression could up-regulate miR-204, inhibit cell apoptosis, promote proliferation and alleviate the oxidative damage of cardiomyocytes induced by CoCl₂.