ArticleMolecular neurobiology2016
Attenuated Reactive Gliosis and Enhanced Functional Recovery Following Spinal Cord Injury in Null Mutant Mice of Platelet-Activating Factor Receptor.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Iron chelation targets lipid metabolism to reduce white matter injury in germinal matrix hemorrhage.Cell death & disease · 2026Article
- Elevated platelet-activating factor levels predict complete brachial plexus injury: a retrospective case-control study.BMC neurology · 2026Article
- IL-18 Blockage Reduces Neuroinflammation and Promotes Functional Recovery in a Mouse Model of Spinal Cord Injury.Biomolecules · 2024Article
- Platelet-Activating Factor Receptor (PAFR) Regulates Retinal Progenitor/Stem Cells Profile in Ciliary Epithelium Cells.International journal of molecular sciences · 2024Article
- Acupuncture combined with moxibustion mitigates spinal cord injury-induced motor dysfunction in mice by NLRP3-IL-18 signaling pathway inhibition.Journal of orthopaedic surgery and research · 2023Article
- Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023Review
- Perinatal methadone exposure attenuates myelination and induces oligodendrocyte apoptosis in neonatal rat brain.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Inhibition of heat shock protein family A member 8 attenuates spinal cord ischemia-reperfusion injury via astrocyte NF-κB/NLRP3 inflammasome pathway : HSPA8 inhibition protects spinal ischemia-reperfusion injury.Journal of neuroinflammation · 2021Article
- Platelet-Activating Factor Deteriorates Lysophosphatidylcholine-Induced Demyelination Via Its Receptor-Dependent and -Independent Effects.Molecular neurobiology · 2020Article
- Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives.Molecules (Basel, Switzerland) · 2019Review
- Dynamic response of microglia/macrophage polarization following demyelination in mice.Journal of neuroinflammation · 2019Article
- RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke.Cell death and differentiation · 2018Article
- Effects of decompression joint Governor Vessel electro-acupuncture on rats with acute upper cervical spinal cord injury.Neural regeneration research · 2018Article
- Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury.Disease models & mechanisms · 2018Article
- Targeting the NLRP3 inflammasome to attenuate spinal cord injury in mice.Journal of neuroinflammation · 2017Article
- Effect of glial cells on remyelination after spinal cord injury.Neural regeneration research · 2017Review
- Current Understanding of Platelet-Activating Factor Signaling in Central Nervous System Diseases.Molecular neurobiology · 2017Review
- Dysfunctional epileptic neuronal circuits and dysmorphic dendritic spines are mitigated by platelet-activating factor receptor antagonism.Scientific reports · 2016Article
- Extrinsic and Intrinsic Regulation of Axon Regeneration by MicroRNAs after Spinal Cord Injury.Neural plasticity · 2016Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
Platelet-activating factor (PAF) is a unique phosphoglycerine that mediates the biological functions of both immune and nervous systems. Excessive PAF plays an important role in neural injury via its specific receptor (PAFR). In this study, we hypothesized that PAF signaling activates reactive gliosis after spinal cord injury (SCI), and blocking the PAF pathway would modify the glia scar formation and promote functional recovery. PAF microinjected into the normal wild-type spinal cord induced a dose-dependent activation of microglia and astrocytes. In the SCI mice, PAFR null mutant mice showed a better functional recovery in grip and rotarod performances than wild-type mice. Although both microglia and astrocytes were activated after SCI in wild-type and PAFR null mutant mice, expressions of IL-6, vimentin, nestin, and GFAP were not significantly elevated in PAFR null mutants. Disruption of PAF signaling inhibited the expressions of proteoglycan CS56 and neurocan (CSPG3). Intriguingly, compared to the wild-type SCI mice, less axonal retraction/dieback at 7 dpi but more NFH-labeled axons at 28 dpi was found in the area adjacent to the epicenter in PAFR null mutant SCI mice. Moreover, treatment with PAFR antagonist Ginkgolide B (GB) at the chronic phase rather than acute phase enhanced the functional recovery in the wild-type SCI mice. These findings suggest that PAF signaling participates in reactive gliosis after SCI, and blocking of this signaling enhances functional recovery and to some extent may promote axon regrowth.
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