Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Abstract

Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects through various regulatory mechanisms. This study aims to investigate the role and molecular mechanism of SNHG11 in Dex-mediated neuroprotection. The ischemic stroke (IS) model was established in vivo by middle cerebral artery occlusion (MCAO) and in vitro by oxygen-glucose deprivation and reperfusion (OGD/R)-treated SH-SY5Y. SNHG11 was highly expressed after OGD/R, and Dex improved OGD/R-induced neurological injury. Additionally, Dex reversed the effects of SNHG11 on OGD/R-induced neurological injury. Furthermore, we found that SNHG11 upregulated vascular endothelial growth factor A (VEGFA) expression by targeting miR-324-3p. Through rescue assays, it was confirmed that SNHG11 regulated OGD/R-induced neurological injury through increasing VEGFA expression. At last, Dex was also discovered to improve neurological injury through regulating SNHG11 in the rat model. In conclusion, our work demonstrated that Dex improved OGD/R-induced neurological injury via SNHG11/miR-324-3p/VEGFA axis. These findings may offer a novel therapeutic strategy for IS treatment.

RETRACTED ARTICLE: LncRNA SOX2-OTinhibitionprotects against myocardialischemia/reperfusion-inducedinjury via themicroRNA-186-5p (miR-186-5p)/Yin Yang 1 (YY1)pathway

“…To construct an OGD/R cell model, H2C9 cardiomyocytes were seeded into glucose-free DMEM and cultivated in the atmosphere containing 95% N 2 and 5% CO 2 for 4 h at 37°C. Thereafter, the H2C9 cells were transferred to fresh normal DMEM containing 4.5 mg/mL glucose and cultured in the regular incubator (95% air+5% CO 2 ) at 37°C for 24 h. Untreated H2C9 cardiomyocytes were used as the Control group [ 14 ].…”

Astrocyte‐like subpopulation of NG2 glia in the adult mouse cortex exhibits characteristics of neural progenitor cells

“…It is therefore possible that the increased expression of both genes shortly after the onset of FCI is related to this neuroprotective function. Similarly, the increased expression of Snhg11 in NG2‐tdTom/Pdgfrα + cells after MCAO may be due to tissue protection, as this gene plays a role in regulating damage caused by oxygen–glucose deprivation/reperfusion in an in vitro model of ischemia (Chen et al, 2021). Sox11 , which was upregulated at later time points after MCAO, was reported to be essential for the initiation of neuronal expression in undifferentiated NPCs (Bergsland et al, 2006).…”

Astrocyte-like subpopulation of NG2 glia in the adult mouse cortex exhibits characteristics of neural progenitor cells and is capable of forming neuron-like cells after ischemic injury

“…It is therefore possible that the increased expression of both genes shortly after the onset of FCI is related to this neuroprotective function. Similarly, the increased expression of Snhg11 in NG2-tdTom/Pdgfrα + cells after MCAO may be due to tissue protection, as this gene plays a role in regulating damage caused by oxygen-glucose deprivation/reperfusion in an in vitro model of ischemia (Chen, Fan, and Wu 2021). Another gene that is upregulated in ischemic tissue shortly after FCI, Sox11 , has been reported to be essential for initiating neuronal expression in undifferentiated NPCs (Bergsland et al 2006).…”