Molecular vision · 2019
MicroRNA-30b regulates the polarity of retinal ganglion cells by inhibiting semaphorin-3A.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Chan-Juan Huang, Sen Lin, Li-Qianyu Ai, Jian Ye, Rong-Di Yuan
Аннотация
PURPOSE: Retinal ganglion cell (RGC) polarity plays an important role in optic nerve regeneration. This study was designed to investigate whether semaphorin-3A (Sema3A) is involved in the regulation of RGC polarity and Sema3A protein expression.
METHODS: Cultured primary RGCs were treated with Fc-Sema3A or Sema3A siRNA or transfected with purified miR-30b recombinant adenoassociated virus (rAAV). The polarity of the RGCs was observed with immunofluorescence. A western blot analysis of phosphorylated protein kinase A (p-PKA), the downstream effector molecule phosphorylated glycogen synthase kinase 3 beta (GSK-3β), and collapsing response mediator protein 2 (CRMP2) was performed.
RESULTS: We found that Sema3A could statistically significantly promote dendritic branching while inhibiting the growth of axons in RGCs. miR-30b overexpression and Sema3A siRNA could statistically significantly promote the growth of axons while inhibiting the growth of dendrites from RGCs. Additionally, miR-30b could restrain the expression of Sema3A protein and its downstream PKA/GSK-3β/CRMP2 signaling pathways.
CONCLUSIONS: The results indicate that Sema3A promotes dendritic growth and inhibits axonal growth, which is not conducive to the early repair of optic nerve injury. The overexpression of miR-30b can overcome this problem, and may represent a new target for the treatment of nerve injury and regeneration in the future.
METHODS: Cultured primary RGCs were treated with Fc-Sema3A or Sema3A siRNA or transfected with purified miR-30b recombinant adenoassociated virus (rAAV). The polarity of the RGCs was observed with immunofluorescence. A western blot analysis of phosphorylated protein kinase A (p-PKA), the downstream effector molecule phosphorylated glycogen synthase kinase 3 beta (GSK-3β), and collapsing response mediator protein 2 (CRMP2) was performed.
RESULTS: We found that Sema3A could statistically significantly promote dendritic branching while inhibiting the growth of axons in RGCs. miR-30b overexpression and Sema3A siRNA could statistically significantly promote the growth of axons while inhibiting the growth of dendrites from RGCs. Additionally, miR-30b could restrain the expression of Sema3A protein and its downstream PKA/GSK-3β/CRMP2 signaling pathways.
CONCLUSIONS: The results indicate that Sema3A promotes dendritic growth and inhibits axonal growth, which is not conducive to the early repair of optic nerve injury. The overexpression of miR-30b can overcome this problem, and may represent a new target for the treatment of nerve injury and regeneration in the future.