LncRNA MALAT1 Promotes Neuronal Apoptosis During Spinal Cord Injury Through miR-199a-5p/ PRDM5 Axis.

Abstract

To determine the regulation of long non-coding RNA (lncRNA) MALAT1 on neuronal apoptosis during spinal cord injury (SCI) and to explore its possible mechanisms. The motor ability of SCI rat models and apoptosis in spinal cord tissue were evaluated. Primary spinal cord neurons (SCNs) were isolated and treated with H2O2 before cell transfection. The apoptosis of SCNs and expression of PRDM5 and MALAT1 were also measured. The interactions among MALAT1, miR-199a-5p, and PRDM5 were detected. The motor ability of SCI rats decreased significantly. The proportion of apoptotic neurons increased in damaged tissue and SCN, along with an increase in the expression of apoptosis-related proteins c-caspase-3/9, autophagy-related proteins (p62 and LC3 II/I ratio), and proinflammatory factors. Moreover, overexpression of MALAT1 and PRDM5 in damaged SCN resulted in an increased apoptosis rate of neurons, elevated expression of apoptosis-related proteins, and upregulated levels of inflammatory factors. However, miR-199a-5p overexpression/PRDM5 knockdown partially counteracted the effects of MALAT1 overexpression on H2O2-induced SCNs. In addition, MALAT1 negatively regulated miR-199a-5p, which targeted PRDM5. LncRNA MALAT1 promotes neuronal apoptosis during SCI by regulating the miR-199a-5p/PRDM5 axis.