ArticleJournal of molecular neuroscience : MN2013
Chemokine CCL2 induces apoptosis in cortex following traumatic brain injury.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Early measurement of interleukin-10 predicts the absence of CT scan lesions in mild traumatic brain injury.PloS one · 2018Trial
- Neuroprotective activity of the α7-nAChR positive allosteric modulator PNU-120596 on short term outcomes after traumatic brain injury.Experimental neurology · 2026Article
- Blood Levels of Dendritic Cell Populations in Patients with Moderate to Severe Traumatic Brain Injury.Neurotrauma reports · 2025Article
- Sex chromosomes and hormones independently influence healthy brain development but act similarly after cranial radiation.Proceedings of the National Academy of Sciences of the United States of America · 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
- Placental growth factor exerts a dual function for cardiomyogenesis and vasculogenesis during heart development.Nature communications · 2023Article
- Multiplex Assessment of Serum Chemokines CCL2, CCL5, CXCL1, CXCL10, and CXCL13 Following Traumatic Brain Injury.Inflammation · 2023Article
- A comparison of the impact on neuronal transcriptome and cognition of rAAV5 transduction with three different doses in the mouse hippocampus.Frontiers in molecular neuroscience · 2023Article
- Article
- Osteopathy in the Cranial Field as a Method to Enhance Brain Injury Recovery: A Preliminary Study.Neurotrauma reports · 2022Article
- The neuroprotection of hyperbaric oxygen therapy against traumatic brain injury via NF-κB/MAPKs-CXCL1 signaling pathways.Experimental brain research · 2022Article
- Pathogenic Functions of Tumor Necrosis Factor Receptor-Frontiers in molecular neuroscience · 2021Article
- Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus.Behavioral and brain functions : BBF · 2020Article
- Bone marrow-derived mesenchymal stem cell transplantation attenuates overexpression of inflammatory mediators in rat brain after cardiopulmonary resuscitation.Neural regeneration research · 2020Article
- Article
- The Potassium SK Channel Activator NS309 Protects Against Experimental Traumatic Brain Injury Through Anti-Inflammatory and Immunomodulatory Mechanisms.Frontiers in pharmacology · 2019Article
- Hyperbaric Oxygen Alleviates the Inflammatory Response Induced by LPS Through Inhibition of NF-κB/MAPKs-CCL2/CXCL1 Signaling Pathway in Cultured Astrocytes.Inflammation · 2018Article
- Effects of estrogen receptor GPR30 agonist G1 on neuronal apoptosis and microglia polarization in traumatic brain injury rats.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018Article
- Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.Nature communications · 2018Article
- Persistent Infiltration and Impaired Response of Peripherally-Derived Monocytes after Traumatic Brain Injury in the Aged Brain.International journal of molecular sciences · 2018Article
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
The chemokine C-C motif ligand 2 (CCL2) is an important mediator of neuroinflammation. Released in response to acute injury, ischemia, and neurodegenerative disease, CCL2 binds primarily to the G-protein-coupled chemokine C-C motif receptor 2 (CCR2) to recruit inflammatory cells to sites of tissue damage. Inflammation is thought to have both beneficial and deleterious consequences following traumatic brain injury (TBI), so we investigated CCL2-CCR2 signaling during the post-TBI period to assess possible neurodegenerative and protective actions. Local TBI in adult rat cortex was induced by Feeney's weight-drop method, and the expression of CCL2 and CCR2 in the tissue around the contusion site was measured by real-time quantitative PCR. Both CCL2 and CCR2 mRNA levels were increased markedly for at least 10 days after injury, peaking on day 3. The CCL2 protein was mainly co-localized with the astroglial marker glial fibrillary acidic protein and CCR2 protein with the neuronal nuclear marker NeuN as revealed by double immunofluorescence staining. A selective CCR2 antagonist, RS504393, reduced TUNEL staining, a marker of apoptosis, and improved performance in the Morris water maze 3 days post-TBI, suggesting that CCL2-CCR2 signaling has deleterious effects on neuronal survival and learning. Targeting the CCL2-CCR2 pathway may provide a novel therapeutic approach for the treatment of TBI.
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