miR-30b Promotes spinal cord sensory function recovery via the Sema3A/NRP-1/PlexinA1/RhoA/ROCK Pathway

Spinal cord injury (SCI) often leads to the loss of motor and sensory functions, placing a burden on patients. This study investigates the potential of miR-30b in promoting the recovery of sensory function after SCI by encouraging the growth of primary sensory neuron (PSN) axons. The research found that miR-30b can target and degrade sema3A mRNA, influencing the sema3A-NRP-1-PlexinA1 complex formation, which is critical for neuronal growth. By regulating this pathway, miR-30b enhances the intrinsic regenerative ability of neurons and promotes neurite growth against inhibitory microenvironments. In vivo experiments showed that miR-30b could regulate the Sema3A/NRP-1/PlexinA1/RhoA/ROCK axis and restore spinal cord sensory conductive function, indicating its potential as a novel target for sensation recovery after SCI.

• 1
  MiR-30b promotes primary sensory neuron axon growth in vitro by targeting and degrading sema3A mRNA.
• 2
  MiR-30b regulates the formation of the sema3A/PlexinA1-NRP-1 complex, influencing intracellular signaling pathways related to axon growth.
• 3
  In vivo experiments confirm that miR-30b can regulate the Sema3A/PlexinA1-NRP-1/RhoA/ROCK pathway after spinal cord dorsal column lesion (SDCL) and promotes sensory conductive function recovery.