ArticleMolecular neurobiology2016
Absence of CCL2 and CCL3 Ameliorates Central Nervous System Grey Matter But Not White Matter Demyelination in the Presence of an Intact Blood-Brain Barrier.
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 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Chemokine Dysregulation and Neuroinflammation in Schizophrenia: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Matrix metalloprotease-9 modulates microglial/macrophage responses in murine brain demyelination.Acta neuropathologica communications · 2026Article
- TRIM21 promotes astrocyte-mediated neuroinflammation in experimental autoimmune encephalomyelitis by stabilizing RGMa via K33-linked ubiquitination.Journal of neuroinflammation · 2026Article
- Exploring the Causal Relationship Between Inflammatory Cytokines and MRI-Derived Brain Iron: A Mendelian Randomization Study.Brain and behavior · 2024Article
- CCL2 Knockdown Attenuates Inflammatory Response After Spinal Cord Injury Through the PI3K/Akt Signaling Pathway: Bioinformatics Analysis and Experimental Validation.Molecular neurobiology · 2024Article
- Article
- Molecular Heterogeneity of the Brain Endothelium.Current issues in molecular biology · 2023Article
- Immune profiling in multiple sclerosis: a single-center study of 65 cytokines, chemokines, and related molecules in cerebrospinal fluid and serum.Frontiers in immunology · 2023Article
- Cuprizone feeding induces swollen astrocyte endfeet.Pflugers Archiv : European journal of physiology · 2022Article
- Article
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Targeting C-C Chemokine Receptor 5: Key to Opening the Neurorehabilitation Window After Ischemic Stroke.Frontiers in cellular neuroscience · 2022Review
- Significant higher-level C-C motif chemokine ligand 2/3 and chemotactic power in cerebral white matter than grey matter in rat and human.The European journal of neuroscience · 2021Article
- Macroglial diversity: white and grey areas and relevance to remyelination.Cellular and molecular life sciences : CMLS · 2021Review
- CCL3 contributes to secondary damage after spinal cord injury.Journal of neuroinflammation · 2020Article
- The role of chemokines and chemokine receptors in multiple sclerosis.International immunopharmacology · 2020Review
- P2x7 receptors control demyelination and inflammation in the cuprizone model.Brain, behavior, & immunity - health · 2020Article
- Dynamic Responses of Microglia in Animal Models of Multiple Sclerosis.Frontiers in cellular neuroscience · 2020Article
- Reboxetine Treatment Reduces Neuroinflammation and Neurodegeneration in the 5xFAD Mouse Model of Alzheimer's Disease: Role of CCL2.Molecular neurobiology · 2019Article
- Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice.Histochemistry and cell biology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A broad spectrum of diseases is characterized by myelin abnormalities, oligodendrocyte pathology, and concomitant glia activation, among multiple sclerosis (MS). Our knowledge regarding the factors triggering gliosis and demyelination is scanty. Chemokines are pivotal for microglia and astrocyte activation and orchestrate critical steps during the formation of central nervous system (CNS) demyelinating lesions. Redundant functions of chemokines complicate, however, the study of their functional relevance. We used the cuprizone model to study redundant functions of two chemokines, CCL2/MCP1 and CCL3/MIP1α, which are critically involved in the pathological process of cuprizone-induced demyelination. First, we generated a mutant mouse strain lacking functional genes of both chemokines and demonstrated that double-mutant animals are viable, fertile, and do not present with gross abnormalities. Astrocytes and peritoneal macrophages, cultured form tissues of these animals did neither express CCL2 nor CCL3. Exposure to cuprizone resulted in increased CCL2 and CCL3 brain levels in wild-type but not mutant animals. Cuprizone-induced demyelination, oligodendrocyte loss, and astrogliosis were significantly ameliorated in the cortex but not corpus callosum of chemokine-deficient animals. In summary, we provide a novel powerful model to study the redundant function of two important chemokines. Our study reveals that chemokine function in the CNS redounds to region-specific pathophysiological events.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.