Abstract
BackgroundCircular RNA (circRNA) is highly expressed in the brain tissue, but its molecular mechanism in cerebral ischemia–reperfusion remains unclear. Here, we explored the role and underlying mechanisms of circRNA antisense non-coding RNA in the INK4 locus (circ_ANRIL) in oxygen–glucose deprivation and reoxygenation (OGD/R)-induced cell injury.ResultsThe expression of circ_ANRIL in OGD/R-induced human brain microvascular endothelial cells (HBMECs) was significantly up-regulated, while that of miR-622 was significantly down-regulated. Overexpression of circ_ANRIL significantly inhibited the proliferation of OGD/R-induced HBMECs and aggravated OGD/R-induced cell apoptosis. Moreover, circ_ANRIL overexpression further increased the secretion of interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 in OGD/R-treated HBMECs. The results of bioinformatics analysis and luciferase reporter assay indicated that circ_ANRIL served as an miR-622 sponge to negatively regulate the expression of miR-622 in OGD/R-treated HBMECs. Additionally, circ_ANRIL silencing exerted anti-apoptotic and anti-inflammatory effects by positively regulating the expression of miR-622. Furthermore, inhibition of OGD/R-induced activation of the nuclear factor (NF)-κB pathway by circ_ANRIL silencing was significantly reversed by treatment with miR-622 inhibitor.ConclusionsKnockdown of circ_ANRIL improved OGD/R-induced cell damage, apoptosis, and inflammatory responses by inhibiting the NF-κB pathway through sponging miR-622.
Highlights
Circular RNA is highly expressed in the brain tissue, but its molecular mechanism in cerebral ischemia–reperfusion remains unclear
Full list of author information is available at the end of the article
Insufficient blood supply followed by blood reperfusion leads to ischemia and reperfusion injury, which is the cause of various complications and deaths associated with stroke, myocardial infarction, and traumatic brain injury [1]
Summary
Circular RNA (circRNA) is highly expressed in the brain tissue, but its molecular mechanism in cerebral ischemia–reperfusion remains unclear. We explored the role and underlying mechanisms of circRNA antisense non-coding RNA in the INK4 locus (circ_ANRIL) in oxygen–glucose deprivation and reoxygenation (OGD/R)-induced cell injury. Insufficient blood supply followed by blood reperfusion leads to ischemia and reperfusion injury, which is the cause of various complications and deaths associated with stroke, myocardial infarction, and traumatic brain injury [1]. Cerebral vascular endothelial cell injury induced by cerebral ischemia–reperfusion (CI/R) is an important cause of brain tissue damage after focal. The mechanism of CI/R injury, a complex pathological process, remains unclear. Effective clinical drugs for the treatment of CI/R injury are still lacking. An in depth understanding of the underlying mechanisms of CI/R injury is important for developing effective treatments
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