miR-182-5p Regulates Nogo-A Expression and Promotes Neurite Outgrowth of Hippocampal Neurons In Vitro.
Altea SotoManuel Nieto-DíazDavid ReigadaMaría Asunción Barreda-MansoTeresa Muñoz-GaldeanoRodrigo M MazaPublished in: Pharmaceuticals (Basel, Switzerland) (2022)
Nogo-A protein is a key myelin-associated inhibitor of axonal growth, regeneration, and plasticity in the central nervous system (CNS). Regulation of the Nogo-A/NgR1 pathway facilitates functional recovery and neural repair after spinal cord trauma and ischemic stroke. MicroRNAs are described as effective tools for the regulation of important processes in the CNS, such as neuronal differentiation, neuritogenesis, and plasticity. Our results show that miR-182-5p mimic specifically downregulates the expression of the luciferase reporter gene fused to the mouse Nogo-A 3'UTR, and Nogo-A protein expression in Neuro-2a and C6 cells. Finally, we observed that when rat primary hippocampal neurons are co-cultured with C6 cells transfected with miR-182-5p mimic, there is a promotion of the outgrowth of neuronal neurites in length. From all these data, we suggest that miR-182-5p may be a potential therapeutic tool for the promotion of axonal regeneration in different diseases of the CNS.
Keyphrases
- spinal cord
- induced apoptosis
- spinal cord injury
- poor prognosis
- stem cells
- blood brain barrier
- cerebral ischemia
- cell cycle arrest
- binding protein
- crispr cas
- endothelial cells
- endoplasmic reticulum stress
- electronic health record
- atrial fibrillation
- machine learning
- genome wide
- long non coding rna
- gene expression
- dna methylation
- white matter
- temporal lobe epilepsy