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. 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. 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. 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.

中文翻译：

---

LncRNA SNHG14通过在HT22小鼠海马神经元细胞中通过miR-182-5p / BINP3轴诱导过量的吞噬作用来促进OGD / R诱导的神经元损伤。

长非编码RNA（lncRNA）小核仁RNA宿主基因14（SNHG14）与脑缺血再灌注（CI / R）损伤相关。这项工作旨在探讨SNHG14在CI / R损伤中的作用。通过氧-葡萄糖剥夺/复氧（OGD / R）处理建立了HT22（小鼠海马神经元细胞）细胞模型。SNHG14，miR-182-5p和BNIP3之间的相互作用已通过荧光素酶报告基因检测得以证实。进行流式细胞术，蛋白质印迹和实时荧光定量PCR检测细胞凋亡，基因和蛋白质的表达。SNHG14和BNIP3高度表达，并且在OGD / R诱导的HT22细胞中miR-182-5p被下调。OGD / R诱导的HT22细胞表现出凋亡增加。SNHG14的过表达促进了OGD / R诱导的HT22细胞的凋亡以及caspase-3和caspase-9的表达。此外，SNHG14上调增强了OGD / R诱导的HT22细胞中BNIP3，Beclin-1和LC3II / LC3I的表达。此外，SNHG14通过使miR-182-5p海绵化来调节BNIP3表达。MiR-182-5p过表达或BNIP3抑制可抑制OGD / R诱导的HT22细胞凋亡，而SNHG14上调则消除了该凋亡。我们的研究表明，lncRNA SNHG14通过在HT22小鼠海马神经元细胞中通过miR-182-5p / BINP3轴诱导过量的自噬来促进OGD / R诱导的神经元损伤。因此，SNHG14 / miR-182-5p / BINP3轴可能是CI / R损伤治疗的重要靶标。MiR-182-5p过表达或BNIP3抑制可抑制OGD / R诱导的HT22细胞凋亡，而SNHG14上调则消除了该凋亡。我们的研究表明，lncRNA SNHG14通过在HT22小鼠海马神经元细胞中通过miR-182-5p / BINP3轴诱导过量的自噬来促进OGD / R诱导的神经元损伤。因此，SNHG14 / miR-182-5p / BINP3轴可能是CI / R损伤治疗的重要靶标。MiR-182-5p过表达或BNIP3抑制可抑制OGD / R诱导的HT22细胞凋亡，而SNHG14上调则消除了该凋亡。我们的研究表明，lncRNA SNHG14通过在HT22小鼠海马神经元细胞中通过miR-182-5p / BINP3轴诱导过量的自噬来促进OGD / R诱导的神经元损伤。因此，SNHG14 / miR-182-5p / BINP3轴可能是CI / R损伤治疗的重要靶标。