ArticleNeurochemical research2020
Integrin CD11b Deficiency Aggravates Retinal Microglial Activation and RGCs Degeneration After Acute Optic Nerve Injury.
Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Integrin CD11b Alleviates Cerebral Ischemia/Reperfusion Injury via a Mechanism Involving Microglia/Macrophage Polarization.Journal of molecular neuroscience : MN · 2025Article
- Tauroursodeoxycholic Acid Protects Retinal Ganglion Cells and Reduces Inflammation in Mice Following Optic Nerve Crush.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Clodronate liposome treatment contributes to the nerve regeneration in corneal nerve involvement of diabetic mice.Experimental animals · 2025Article
- ATF3 prevents retinal ganglion cell apoptosis and mitigates microglia-mediated neuroinflammation in retinal ischemia-reperfusion injury.Frontiers in immunology · 2025Article
- Article
- The integrin CD11b inhibits MSU-induced NLRP3 inflammasome activation in macrophages and protects mice against MSU-induced joint inflammation.Arthritis research & therapy · 2024Article
- Effect of astrocyte GPER on the optic nerve inflammatory response following optic nerve injury in mice.Heliyon · 2024Article
- Ablation of the integrin CD11b mac-1 limits deleterious responses to traumatic spinal cord injury and improves functional recovery in mice.Research square · 2024Article
- Physcion prevents induction of optic nerve injury in rats via inhibition of the JAK2/STAT3 pathway.Experimental and therapeutic medicine · 2023Article
- The role of monocytes in optic nerve injury.Neural regeneration research · 2023Review
- 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
- Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Axonal Injuries Cast Long Shadows: Long Term Glial Activation in Injured and Contralateral Retinas after Unilateral Axotomy.International journal of molecular sciences · 2021Article
- Semaphorin3A increases M1-like microglia and retinal ganglion cell apoptosis after optic nerve injury.Cell & bioscience · 2021Article
- Modulation of Sirt1-mTORC1 Pathway in Microglia Attenuates Retinal Ganglion Cell Loss After Optic Nerve Injury.Journal of inflammation research · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroinflammation plays a vital role in the process of a variety of retinal ganglion cells (RGCs) degenerative diseases including traumatic optic neuropathy (TON). Retinal microglial activation is believed as a harbinger of TON, and robust microglial activation can aggravate trauma-induced RGCs degeneration, which ultimately leads to RGCs loss. Toll like receptor 4 (TLR4)-triggered inflammation is of great importance in retinal inflammatory response after optic nerve injury. CD11b on macrophage and brain microglia can inhibit TLR4-triggered inflammation. However, the functional role of CD11b in retinal microglia is not well understood. Here, using an optic nerve crush model and CD11b gene deficient mice, we found that CD11b protein expression was mainly on retinal microglia, significantly increased after optic nerve injury, and still maintained at a high level till at least 28 days post crush. Compared with wild type mice, following acute optic nerve injury, CD11b deficient retinae exhibited more exacerbated microglial activation, accelerated RGCs degeneration, less growth associated protein-43 expression, as well as more proinflammatory cytokines such as interleukin-6 and tumor necrosis factor α while less anti-inflammatory factors such as arginase-1 and interleukin-10 production. We conclude that CD11b is essential in regulating retinal microglial activation and neuroinflammatory responses after acute optic nerve injury, which is critical for subsequent RGCs degeneration and loss.
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Registered trials
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