ArticleCell & bioscience2021
Semaphorin3A increases M1-like microglia and retinal ganglion cell apoptosis after optic nerve injury.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 31 citations in OpenAlex.
- Extrinsic Regulation of Optic Nerve Axon Regeneration in the Adult Central Nervous System.Cells · 2026Review
- Myeloid HDAC3 deletion protects against traumatic optic injury.Cell death discovery · 2026Article
- Preserving blood-retinal barrier integrity: a path to retinal ganglion cell protection in glaucoma and traumatic optic neuropathy.Cell regeneration (London, England) · 2025Review
- Engineered bio-functional material-based nerve guide conduits for optic nerve regeneration: a view from the cellular perspective, challenges and the future outlook.Regenerative biomaterials · 2025Review
- Understanding amblyopia from the perspective of neurovascular units: changes in the retina and brain.Frontiers in cell and developmental biology · 2025Review
- Implantation of biomimetic polydopamine nanocomposite scaffold promotes optic nerve regeneration through modulating inhibitory microenvironment.Journal of nanobiotechnology · 2024Article
- Influence of dexamethasone-induced matrices on the TM transcriptome.Experimental eye research · 2024Article
- Toward discovering a novel family of peptides targeting neuroinflammatory states of brain microglia and astrocytes.Journal of neurochemistry · 2024Article
- Microglial CD11b Knockout Contributes to Axonal Debris Clearance and Axonal Degradation Attenuation via IGF-1 After Acute Optic Nerve Injury.Investigative ophthalmology & visual science · 2023Article
- Molecular, cellular and neurological consequences of infection by the neglected human pathogen Nocardia.BMC biology · 2022Article
- An increase in Semaphorin 3A biases the axonal direction and induces an aberrant dendritic arborization in an in vitro model of human neural progenitor differentiation.Cell & bioscience · 2022Article
- Neuroinflammation, Microglia and Implications for Retinal Ganglion Cell Survival and Axon Regeneration in Traumatic Optic Neuropathy.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mechanisms leading to retinal ganglion cell (RGC) death after optic nerve injury have not been fully elucidated. Current evidence indicates that microglial activation and M1- and M2-like dynamics may be an important factor in RGC apoptosis after optic nerve crush (ONC). Semaphorin3A (Sema3A) is a classic axonal guidance protein,which has been found to have a role in neuroinflammation processes. In this study, we investigated the contribution of microglial-derived Sema3A to progressive RGC apoptosis through regulating paradigm of M1- and M2-like microglia after ONC.
methodA mouse ONC model and a primary microglial-RGC co-culture system were used in the present study. The expression of M1- and M2-like microglial activation markers were assessed by real-time polymerase chain reaction (RT-qPCR). Histological and Western blot (WB) analyses were used to investigate the polarization patterns of microglia transitions and the levels of Sema3A. RGC apoptosis was investigated by TUNEL staining and caspase-3 detection.
resultsLevels of Sema3A in the mouse retina increased after ONC. Treatment of mice with the stimulating factor 1 receptor antagonist PLX3397 resulted in a decrease of retinal microglia. The levels of CD16/32 (M1) were up-regulated at days 3 and 7 post-ONC. However, CD206 (M2) declined on day 7 after ONC. Exposure to anti-Sema3A antibodies (anti-Sema3A) resulted in a decrease in the number of M1-like microglia, an increase in the number of M2-like microglia, and the amelioration of RGC apoptosis.
conclusionsAn increase in microglia-derived Sema3A in the retina after ONC partially leads to a continuous increase of M1-like microglia and plays an important role in RGC apoptosis. Inhibition of Sema3A activity may be a novel approach to the prevention of RGC apoptosis after optic nerve injury.
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