ArticleMolecular vision2019
MicroRNA-30b regulates the polarity of retinal ganglion cells by inhibiting semaphorin-3A.
Article in Molecular vision, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Chitosan/PLGA-based tissue engineered nerve grafts with SKP-SC-EVs enhance sciatic nerve regeneration in dogs through miR-30b-5p-mediated regulation of axon growth.Bioactive materials · 2024Article
- ADSC-Exos outperform BMSC-Exos in alleviating hydrostatic pressure-induced injury to retinal ganglion cells by upregulating nerve growth factors.World journal of stem cells · 2023Article
- Article
- Efficacy of an Anti-Semaphorin 3A Neutralizing Antibody in a Male Experimental Retinal Vein Occlusion Mouse Model.Investigative ophthalmology & visual science · 2022Article
- Synaptic or Non-synaptic? Different Intercellular Interactions with Retinal Ganglion Cells in Optic Nerve Regeneration.Molecular neurobiology · 2022Review
- Modelling and Refining Neuronal Circuits with Guidance Cues: Involvement of Semaphorins.International journal of molecular sciences · 2021Review
- Semaphorin3A increases M1-like microglia and retinal ganglion cell apoptosis after optic nerve injury.Cell & bioscience · 2021Article
- Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
31814697PMC6857778W2995835785What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.