ArticleExperimental neurology2014
Osteopontin expression in acute immune response mediates hippocampal synaptogenesis and adaptive outcome following cortical brain injury.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Vagus nerve stimulation inhibits pyroptosis and improves outcome of cerebral ischemic stroke by upregulating osteopontin (SPP1) to disturb ASC oligomerization.BMC medicine · 2025Article
- The potential link between the development of Alzheimer's disease and osteoporosis.Biogerontology · 2025Review
- Blockade of brain alkaline phosphatase efficiently reduces amyloid-β plaque burden and associated cognitive impairment.Alzheimer's research & therapy · 2024Article
- Proteomics identifies lipocalin-2 in neonatal inflammation associated with cerebrovascular alteration in mice and preterm infants.iScience · 2023Article
- Article
- Osteopontin depletion in macrophages perturbs proteostasisFrontiers in immunology · 2023Article
- Osteopontin - The stirring multifunctional regulatory factor in multisystem aging.Frontiers in endocrinology · 2022Review
- Morphological and biomolecular targets in retina and vitreous from Reelin-deficient mice (Reeler): Potential implications for age-related macular degeneration in Alzheimer's dementia.Frontiers in aging neuroscience · 2022Article
- Review
- Quantitative Proteomics Reveals the Dynamic Pathophysiology Across Different Stages in a Rat Model of Severe Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Article
- Review
- Patterns of Osteopontin Expression in Abusive Head Trauma Compared with Other Causes of Pediatric Traumatic Brain Injury.The Journal of pediatrics · 2020Article
- Multi-Dimensional Mapping of Brain-Derived Extracellular Vesicle MicroRNA Biomarker for Traumatic Brain Injury Diagnostics.Journal of neurotrauma · 2020Article
- Repetitive Mild Traumatic Brain Injury and Transcription Factor Modulation.Journal of neurotrauma · 2020Article
- DHA Attenuates Cerebral Edema Following Traumatic Brain Injury via the Reduction in Blood-Brain Barrier Permeability.International journal of molecular sciences · 2020Article
- Neutralization of Lipocalin-2 Diminishes Stroke-Reperfusion Injury.International journal of molecular sciences · 2020Article
- Osteopontin as a candidate of therapeutic application for the acute brain injury.Journal of cellular and molecular medicine · 2020Review
- Osteopontin and Integrin Mediated Modulation of Post-Synapses in HIV Envelope Glycoprotein Exposed Hippocampal Neurons.Brain sciences · 2020Article
- Plasma osteopontin may predict neuroinflammation and the severity of pediatric traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Activated Bone Marrow-Derived Macrophages Eradicate Alzheimer's-Related AβFrontiers in immunology · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) produces axotomy, deafferentation and reactive synaptogenesis. Inflammation influences synaptic repair, and the novel brain cytokine osteopontin (OPN) has potential to support axon regeneration through exposure of its integrin receptor binding sites. This study explored whether OPN secretion and proteolysis by matrix metalloproteinases (MMPs) mediate the initial degenerative phase of synaptogenesis, targeting reactive neuroglia to affect successful repair. Adult rats received unilateral entorhinal cortex lesion (UEC) modeling adaptive synaptic plasticity. Over the first week postinjury, hippocampal OPN protein and mRNA were assayed and histology was performed. At 1-2d, OPN protein increased up to 51 fold, and was localized within activated, mobilized glia. OPN transcript also increased over 50 fold, predominantly within reactive microglia. OPN fragments known to be derived from MMP proteolysis were elevated at 1d, consistent with prior reports of UEC glial activation and enzyme production. Postinjury minocycline immunosuppression attenuated MMP-9 gelatinase activity, which was correlated with the reduction of neutrophil gelatinase-associated lipocalin (LCN2) expression, and reduced OPN fragment generation. The antibiotic also attenuated removal of synapsin-1 positive axons from the deafferented zone. OPN KO mice subjected to UEC had similar reduction of hippocampal MMP-9 activity, as well as lower synapsin-1 breakdown over the deafferented zone. MAP1B and N-cadherin, surrogates of cytoarchitecture and synaptic adhesion, were not affected. OPN KO mice with UEC exhibited time dependent cognitive deficits during the synaptogenic phase of recovery. This study demonstrates that OPN can mediate immune response during TBI synaptic repair, positively influencing synapse reorganization and functional recovery.
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