Long non-coding RNA SNHG7 upregulates FGF9 to alleviate oxygen and glucose deprivation-induced neuron cell injury in a miR-134-5p-dependent manner.

Abstract

Long non-coding RNA small nucleolar RNA host gene 7 (SNHG7) was reported to regulate the pathogenesis of ischemic stroke. The study aimed to disclose SNHG7 role in oxygen and glucose deprivation (OGD)-induced Neuro-2a (N2a) cell disorders. An OGD injury cell model was established using N2a cells. The expression of SNHG7, microRNA-134-5p (miR-134-5p) and fibroblast growth factor 9 (FGF9) was determined by quantitative real-time polymerase chain reaction. Protein expression was detected by western blot. Cell viability and Lactate Dehydrogenase (LDH) leakage were determined by cell counting kit-8 and LDH activity detection assays. Oxidative stress was investigated by Superoxide Dismutase and Catalase activity assays as well as Malondialdehyde and Reactive Oxygen Species detection kits. Cell apoptosis and caspase-3 activity were severally demonstrated by flow cytometry and caspase-3 activity assays. The interaction between miR-134-5p and SNHG7 or FGF9 was predicted by online databases, and identified by mechanism assays. OGD treatment decreased SNHG7 and FGF9 expression, but increased miR-134-5p expression. OGD treatment repressed cell viability, promoted LDH leakage and induced oxidative stress and apoptosis in N2a cells, which was rescued by SNHG7 overexpression. SNHG7 acted as a sponge for miR-134-5p, and regulated OGD-triggered cell damage by associating with miR-134-5p. Additionally, miR-134-5p depletion protected N2a cells from OGD-induced injury by targeting FGF9. Ectopic SNHG7 expression protected against OGD-induced neuronal cell injury by inducing FGF9 through sponging miR-134-5p, providing a novel therapeutic target for ischemic stroke.