Depleted histone deacetylase 3 or restored microRNA-19b-1-5p facilitates recovery of spinal cord injury via inactivating JAK2/STAT3 signaling pathway

We intended to discuss the influence of histone deacetylase 3 (HDAC3) on spinal cord injury (SCI) by regulating microRNA-19b-1-5p (miR-19b-1-5p) and janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. In a rat model, the role of HDAC3 and miR-19b-1-5p in SCI was identified through detecting motor function, serum inflammation, pathological damage, cell apoptosis and GFAP expression. Also, by measuring GFAP expression and migration of spinal cord astrocytes, the effects of HDAC3 and miR-19b-1-5p in SCI were identified in vitro. Restoration of miR-19b-1-5p or depletion of HDAC3 alleviated motor function, inflammation, relieved pathological damage and reduced apoptosis, and reduced GFAP expression in the spinal cord tissue of SCI rats. Up-regulating miR-19b-1-5p or down-regulating HDAC3 decreased migration and GFAP expression of injured astrocytes. Our study presents that down-regulated HDAC3 can facilitate the recovery of SCI via inhibiting the activation of JAK2/STAT3 pathway by up-regulating miR-19b-1-5p.

Automated summary

This study reveals that down-regulation of HDAC3 can promote the recovery of SCI by regulating miR-19b-1-5p and inhibiting the activation of JAK2/STAT3 pathway, leading to improvements in inflammation, pathological damage, apoptosis, and GFAP expression.