ArticleFrontiers in cellular neuroscience2014
Schwann cell-derived Apolipoprotein D controls the dynamics of post-injury myelin recognition and degradation.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The Lipocalin Apolipoprotein D Functional Portrait: A Systematic Review.Frontiers in physiology · 2021Pooled it
- Apolipoprotein D Expression Dynamics During Cuprizone-Induced Demyelination and Remyelination in a Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2025Article
- Role and Diagnostic Significance of Apolipoprotein D in Selected Neurodegenerative Disorders.Diagnostics (Basel, Switzerland) · 2024Review
- The Link Between Paraquat and Demyelination: A Review of Current Evidence.Antioxidants (Basel, Switzerland) · 2024Review
- Astrocyte-derived apolipoprotein D is required for neuronal survival in Parkinson's disease.NPJ Parkinson's disease · 2024Article
- Apolipoprotein D as a Potential Biomarker in Neuropsychiatric Disorders.International journal of molecular sciences · 2023Review
- Insulin-degrading enzyme (IDE) as a modulator of microglial phenotypes in the context of Alzheimer's disease and brain aging.Journal of neuroinflammation · 2023Article
- Promotion effect of TGF-β-Zfp423-ApoD pathway on lip sensory recovery after nerve sacrifice caused by nerve collateral compensation.International journal of oral science · 2023Article
- Apolipoprotein D in Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Dual role of Apolipoprotein D as long-term instructive factor and acute signal conditioning microglial secretory and phagocytic responses.Frontiers in cellular neuroscience · 2023Article
- Review: Myelin clearance is critical for regeneration after peripheral nerve injury.Frontiers in neurology · 2022Review
- Cerebral Apolipoprotein D Exits the Brain and Accumulates in Peripheral Tissues.International journal of molecular sciences · 2021Article
- Apolipoprotein D.Gene · 2020Review
- Redefining the heterogeneity of peripheral nerve cells in health and autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Lipid-Binding Proteins in Brain Health and Disease.Frontiers in neurology · 2019Review
- Modeling the Pathogenesis of Charcot-Marie-Tooth Disease Type 1A Using Patient-Specific iPSCs.Stem cell reports · 2018Article
- Extracellular Vesicles Secreted by Astroglial Cells Transport Apolipoprotein D to Neurons and Mediate Neuronal Survival Upon Oxidative Stress.Frontiers in cellular neuroscience · 2018Article
- Expression Pattern of Myelin-Related Apolipoprotein D in Human Multiple Sclerosis Lesions.Frontiers in aging neuroscience · 2018Article
- Apolipoprotein D Concentration in Human Plasma during Aging and in Parkinson's Disease: A Cross-Sectional Study.Parkinson's disease · 2018Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Management of lipids, particularly signaling lipids that control neuroinflammation, is crucial for the regeneration capability of a damaged nervous system. Knowledge of pro- and anti-inflammatory signals after nervous system injury is extensive, most of them being proteins acting through well-known receptors and intracellular cascades. However, the role of lipid binding extracellular proteins able to modify the fate of lipids released after injury is not well understood. Apolipoprotein D (ApoD) is an extracellular lipid binding protein of the Lipocalin family induced upon nervous system injury. Our previous study shows that axon regeneration is delayed without ApoD, and suggests its participation in early events during Wallerian degeneration. Here we demonstrate that ApoD is expressed by myelinating and non-myelinating Schwann cells and is induced early upon nerve injury. We show that ApoD, known to bind arachidonic acid (AA), also interacts with lysophosphatidylcholine (LPC) in vitro. We use an in vivo model of nerve crush injury, a nerve explant injury model, and cultured macrophages exposed to purified myelin, to uncover that: (i) ApoD regulates denervated Schwann cell-macrophage signaling, dampening MCP1- and Tnf-dependent macrophage recruitment and activation upon injury; (ii) ApoD controls the over-expression of the phagocytosis activator Galectin-3 by infiltrated macrophages; (iii) ApoD controls the basal and injury-triggered levels of LPC and AA; (iv) ApoD modifies the dynamics of myelin-macrophage interaction, favoring the initiation of phagocytosis and promoting myelin degradation. Regulation of macrophage behavior by Schwann-derived ApoD is therefore a key mechanism conditioning nerve injury resolution. These results place ApoD as a lipid binding protein controlling the signals exchanged between glia, neurons and blood-borne cells during nerve recovery after injury, and open the possibility for a therapeutic use of ApoD as a regeneration-promoting agent.
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