Abstract
BackgroundLong non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) is associated with cerebral ischemia–reperfusion (CI/R) injury. This work aims to explore the role of SNHG14 in CI/R injury.MethodsHT22 (mouse hippocampal neuronal cells) cell model was established by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. The interaction among SNHG14, miR-182-5p and BNIP3 was verified by luciferase reporter assay. Flow cytometry, western blot and quantitative real-time PCR were performed to examine apoptosis, the expression of genes and proteins.ResultsSNHG14 and BNIP3 were highly expressed, and miR-182-5p was down-regulated in the OGD/R-induced HT22 cells. OGD/R-induced HT22 cells exhibited an increase in apoptosis. SNHG14 overexpression promoted apoptosis and the expression of cleaved-caspase-3 and cleaved-caspase-9 in the OGD/R-induced HT22 cells. Moreover, SNHG14 up-regulation enhanced the expression of BNIP3, Beclin-1, and LC3II/LC3I in the OGD/R-induced HT22 cells. Furthermore, SNHG14 regulated BNIP3 expression by sponging miR-182-5p. MiR-182-5p overexpression or BNIP3 knockdown repressed apoptosis in OGD/R-induced HT22 cells, which was abolished by SNHG14 up-regulation.ConclusionOur study demonstrates that lncRNA SNHG14 promotes OGD/R-induced neuron injury by inducing excessive mitophagy via miR-182-5p/BINP3 axis in HT22 mouse hippocampal neuronal cells. Thus, SNHG14/miR-182-5p/BINP3 axis may be a valuable target for CI/R injury therapies.
Highlights
Long non-coding RNA small nucleolar RNA host gene 14 (SNHG14) is associated with cerebral ischemia–reperfusion (CI/R) injury
The modified HT22 cells were subjected to oxygen–glucose deprivation (OGD)/R treatment. b QRT-PCR was performed to detect the expression of SNHG14 in the modified HT22 cells. c Flow cytometry was performed to explore the apoptosis of the modified HT22 cells. d The expression of caspase-3, cleaved-caspase-3, caspase-9 and cleaved-caspase-9 in the modified HT22 cells was examined by Western blot (WB). (*P < 0.05, **P < 0.01, versus Control or Vector; #P < 0.05, ##P < 0.01, versus si-Ctrl) instruction
SNHG14 overexpression promotes apoptosis of OGD/ R‐induced HT22 cells To investigate the role of SNHG14 in cerebral ischemia– reperfusion injury, HT22 cells were subjected to oxygen–glucose deprivation/ reoxygenation (OGD/R) treatment
Summary
Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) is associated with cerebral ischemia–reperfusion (CI/R) injury. This work aims to explore the role of SNHG14 in CI/R injury. Cerebral ischemia–reperfusion (CI/R) injury is an extremely complex pathophysiological process, showing a rapid cascade reaction. Cerebral ischemic injury induces the expression of inflammatory cytokines and inflammatory cell infiltration, which in turn causes. Recent study has reported that electroacupuncture improves CI/R injury by activating Pink1/Parkin-induced mitophagy [7]. Bcl-2/E1B 19 kDa-interacting protein 3 (BNIP3) is highly expressed after CI/R, which causes excessive activation of mitophagy, triggers delayed cell death, and aggravates CI/R injury [9]. These findings show that mitophagy is a double-edged sword. In-depth study of mitophagy can better analyze the pathological process of CI/R injury
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