LncRNA SNHG5 enhances astrocytes and microglia viability via upregulating KLF4 in spinal cord injury.

This study aims to explore the role and mechanism of lncRNA SNHG5 in spinal cord injury (SCI). The interaction between SNHG5 and Krüppel-like factor 4 (KLF4) was verified by RNA pull-down and RNA immunoprecipitation (RIP) assay. Rat neural function was evaluated by BBB and BMS scores. Results showed that GFAP and Iba-1 (specific proteins for astrocytes and microglia respectively) were upregulated in spinal cord of SCI rats. Simultaneously, spinal cord also expressed substantially higher levels of SNHG5, KLF4 and eNOS (endothelial Nitric Oxide Synthase) than sham group. In traumatically injured astrocytes and microglia, SNHG5 overexpression increased cells viability, which was significantly inhibited by SNHG5 knockdown. KLF4 is a directly target for SNHG5 and is positively regulated by SNHG5. The knockdown of KLF4 effectively decreased astrocytes and microglia viability induced by SHNG5 overexpression and attenuated the pcDNA-SNHG5-mediated repression of the apoptosis. In SCI rats, the injection of Lenti-SNHG5 reduced BBB and BMS scores and also enhanced the protein expression of KLF4, eNOS, GFAP and Iba-1. In summary, our data suggested that SNHG5 promotes SCI via increasing the viability of astrocytes and microglia. The mechanism by which SNHG5 works is its directive interaction to KLF4 and contribution to eNOS upregulation.