ArticleGlia2012
The CCL2-CCR2 system affects the progression and clearance of intracerebral hemorrhage.
Article in Glia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 97 citations in OpenAlex.
- Interleukin-1 regulates myeloid cell trafficking and cerebral blood flow following intracerebral haemorrhage.Disease models & mechanisms · 2025Article
- CXCR3-mediated natural killer cell infiltration exacerbates white matter injury after intracerebral haemorrhage.Brain : a journal of neurology · 2025Article
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- A dispensable role of mural cell-derived laminin-Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- P2Y6 Receptor Activation Aggravates NLRP3-dependent Microglial Pyroptosis via Downregulation of the PI3K/AKT Pathway in a Mouse Model of Intracerebral Hemorrhage.Molecular neurobiology · 2024Article
- CC Chemokine Family Members' Modulation as a Novel Approach for Treating Central Nervous System and Peripheral Nervous System Injury-A Review of Clinical and Experimental Findings.International journal of molecular sciences · 2024Review
- New Insights into Roles of IL-7R Gene as a Therapeutic Target Following Intracerebral Hemorrhage.Journal of inflammation research · 2024Article
- Amyloid-β (Aβ) immunotherapy induced microhemorrhages are associated with activated perivascular macrophages and peripheral monocyte recruitment in Alzheimer's disease mice.Molecular neurodegeneration · 2023Article
- Association between platelet-lymphocyte ratio and 90-day mortality in patients with intracerebral hemorrhage: data from the MIMIC-III database.Frontiers in neurology · 2023Article
- Fibroblasts repair blood-brain barrier damage and hemorrhagic brain injury via TIMP2.Cell reports · 2022Article
- Review
- Lipoxin ABrain sciences · 2022Article
- The roles of chemokines following intracerebral hemorrhage in animal models and humans.Frontiers in molecular neuroscience · 2022Review
- MCP-1: Function, regulation, and involvement in disease.International immunopharmacology · 2021Review
- Distinct peripheral blood monocyte and neutrophil transcriptional programs following intracerebral hemorrhage and different etiologies of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Microglia-derived interleukin-10 accelerates post-intracerebral hemorrhage hematoma clearance by regulating CD36.Brain, behavior, and immunity · 2021Article
- Time Course of Peripheral Leukocytosis and Clinical Outcomes After Aneurysmal Subarachnoid Hemorrhage.Frontiers in neurology · 2021Article
- Age-related CCL12 Aggravates Intracerebral Hemorrhage-induced Brain Injury via Recruitment of Macrophages and T Lymphocytes.Aging and disease · 2020Article
- Loss of mural cell-derived laminin aggravates hemorrhagic brain injury.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Intracerebral hemorrhage (ICH) has been associated with inflammation and apoptosis. The CCL2-CCR2 chemotactic system is one of the major signaling pathways that induce inflammation and apoptosis. However, its role on ICH has not been investigated. We subjected wild-type, CCL2(-/-) , and CCR2(-/-) mice to collagenase-induced ICH, and assessed histological and behavioral outcomes. Lack of CCL2 or CCR2 decreased the hematoma volume early after collagenase-induced ICH but delayed its recovery. The hematoma size was accompanied by brain edema, neuronal death, and neurological scores. Although microglia activation/migration was attenuated in CCL2(-/-) or CCR2(-/-) mice 1 day after injury, more microglia were present at later time points, suggesting that alternative signaling pathways had been activated to recruit them. On the contrary, leukocyte and neutrophil infiltration were decreased in these mice, suggesting a tighter/recovered blood-brain barrier. In addition, we also found that FL- and K104Stop-CCL2 were able to restore the changes found in CCL2(-/-) mice, but K104A-CCL2 failed to do so. These results suggest that plasmin-mediated truncation of CCL2 may be an indispensable step to fully activate the chemokine in vivo. The data also indicate that CCL2-CCR2 signaling pathway may be a molecular target for the treatment of ICH.
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What OpenQuestion holds
Registered trials
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.