AIM  To investigate the effect of long non-coding RNA (lnc RNA) nucleolar RNA host gene 15 (SNHG15) on hypoxia-induced cardiomyocyte injury through miR-24-3p.

  METHODS  The expressions of SNHG15 and miR-24-3p in hypoxia-induced cardiomyocytes were detected by RT-qPCR. The cells were divided into control group, hypoxia group, hypoxia+si-SNHG15 group, hypoxia+si-NC group, hypoxia+miR-24-3p inh group, hypoxia+inh-NC group and si-SNHG15+miR-24-3p inh group. The effects of SNHG15 and miR-24-3p on cardiomyocyte proliferation, apoptosis and migration were detected by MTT, flow cytometry, Caspase-3 kit and Transwell. Objective gene was predicted and screened, luciferase reporter gene was detected to verify the downstream target genes of SNHG15 and miR-24-3p, and the expressions of Atg12 protein and related autophagy genes were detected by Western blotting.

  RESULTS  With the prolongation of the duration of hydrogen peroxide, the level of SNHG15 in cardiomyocytes increased significantly, while the level of miRNA-24-3p decreased in a time-dependent manner. Compared with those in the control group, the cell viability, migration and invasiveness of hypoxia group were significantly decreased, while Caspase-3 activity and apoptosis rate were significantly increased. Compared with those in hypoxia group, the cell viability, migration and invasiveness of hypoxia+si-SNHG15 group were significantly higher, while Caspase-3 activity and apoptosis rate were significantly lower than those in hypoxia+si-SNHG15 group. There was a negative correlation between miR-24-3p and SNHG15. The possible targets of miR24-3p, SNHG15 and Atg12 were predicted by online software. The results of luciferase detection showed that there was a targeted regulation relationship between miR-24-3p and SNHG15 and Atg12. Compared with those in hypoxia group, cell viability, migration and invasiveness in hypoxia+miR-24-3p inh group decreased significantly, while Caspase-3 activity and apoptosis rate increased significantly (P<0.05). Compared with those in hypoxia+miR-24-3p inh group, cell viability, migration and invasiveness in si-SNHG15+miR-24-3p inh group increased significantly, while Caspase-3 activity and apoptosis rate decreased significantly (P<0.05). Compared with those in control group, the expressions of Atg12 and LC3 protein in hypoxia group were significantly up-regulated, while the expression of p62 was significantly down-regulated in hypoxia+miR-24-3p inh group. Compared with those in hypoxia group, the expressions of Atg12 protein and LC3 in hypoxia+miR-24-3p inh group were significantly up-regulated, and p62 expression was significantly down-regulated in si-SNHG15+miR-24-3p inh group compared with that in hypoxia+miR-24-3p inh group (P<0.05). Compared with those in hypoxia+miR-24-3p inh group, the expressions of Atg12 protein and LC3 were significantly down-regulated, and the expression of p62 was significantly up-regulated in si-SNHG15+miR-24-3p inh group.

  CONCLUSION  lnc RNA SNHG15 regulates the proliferation of cardiomyocytes by regulating miR-24-3p/Atg12 axis, thus accelerating the occurrence and development of cardiomyocytes.