4.6 Article

LncRNA SNHG14 promotes OGD/R-induced neuron injury by inducing excessive mitophagy via miR-182-5p/BINP3 axis in HT22 mouse hippocampal neuronal cells

期刊

BIOLOGICAL RESEARCH
卷 53, 期 1, 页码 -

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SOC BIOLGIA CHILE
DOI: 10.1186/s40659-020-00304-4

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SNHG14; miR-182-5p; BINP3; Mitophagy; Cerebral ischemia-reperfusion injury

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资金

  1. Changsha Natural Science Foundation of China [kq2001043]

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Background 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. Methods HT22 (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. Results SNHG14 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. Conclusion Our 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.

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