Journal
NEUROTOXICITY RESEARCH
Volume 40, Issue 2, Pages 542-552Publisher
SPRINGER
DOI: 10.1007/s12640-022-00485-8
Keywords
FTX; miR-186-5p; MDM4; Cerebral ischemia-reperfusion injury; Apoptosis
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This study found that the lncRNA FTX can improve cerebral ischemia-reperfusion injury by regulating the miR-186-5p/MDM4 pathway, providing a new therapeutic strategy for stroke impairment treatment.
LncRNA five prime to Xist (FTX) has been identified to exert a protective effect in multiple diseases. However, whether and how FTX attenuates cerebral ischemia-reperfusion injury (CI/RI) is still unclear. To simulate CI/RI, an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) HT22 cell model and an in vivo middle cerebral artery occlusion/reperfusion (MCAO/R) Sprague-Dawley rat model were respectively constructed. In CI/RI plasma samples, OGD/R-challenged HT22 cells, and brain tissues from MCAO/R rats, FTX and mouse double minute 4 (MDM4) expressions were substantially decreased while miR-186-5p abundance was evidently increased. It was also revealed that FTX obviously improved neuronal damage induced by OGD/R through increasing proliferation, reducing apoptosis, and alleviating oxidative stress in OGD/R-challenged HT22 cells. Additionally, FTX positively regulated MDM4 level in OGD/R-treated HT22 cells as a sponge of miR-186-5p. Moreover, miR-186-5p upregulation or MDM4 suppression restored the inhibitory effects of FTX upregulation on OGD/R-triggered neuronal damage in HT22 cells. Therefore, these results suggest that FTX might ameliorate CI/RI by regulating the miR-186-5p/MDM4 pathway, providing a new target for stroke impairment treatment.
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