| First Author | Ma Q | Year | 2020 |
| Journal | Apoptosis | Volume | 25 |
| Issue | 5-6 | Pages | 400-411 |
| PubMed ID | 32385693 | Mgi Jnum | J:346259 |
| Mgi Id | MGI:6874261 | Doi | 10.1007/s10495-020-01606-4 |
| Citation | Ma Q, et al. (2020) The function of RNase L and its degradation mechanism in cardiac acute ischemic injury. Apoptosis 25(5-6):400-411 |
| abstractText | RNase L is generally thought to play a key role in antiviral defenses. Although RNase L protein and mRNA are known to be highly expressed in myocardial tissue, there are few studies of the potential functions of RNase L in myocardial tissue. In this study, we tested the hypothesis that RNase L may be involved in the pathological process of cardiac ischemic injury. RNase L-overexpressing and RNase L knockdown H9c2 cell lines were subjected to the oxygen and glucose deprivation (OGD) model, and RNase L knockout mice were subjected to acute myocardial infarction surgical procedures to investigate the function of RNase L in ischemic heart injury. OGD induced abnormal aggregation of double-stranded RNA in H9c2 cells, activated RNase L within 6 h of OGD initiation, and mediated apoptosis via the c-Jun N-terminal kinase pathway. In addition, RNase L knockout mice were more tolerant of myocardial infarction, and this knockout protected heart function and prevented pathological ventricular remodeling. Notably, both in in vivo and in vitro experiments, RNase L was gradually diminished during prolonged ischemic injury, which we speculate is an adaptive protective response serving to reduce myocardial ischemic damage. These results suggest that RNase L plays a role in the pathological process of cardiac acute ischemic injury. It is first activated by ischemic injury, causing cardiomyocyte death, but gradually diminishes to protect the heart from further damage. |
