ArticleInternational journal of molecular medicine2019
Expression changes of CX3CL1 and CX3CR1 proteins in the hippocampal CA1 field of the gerbil following transient global cerebral ischemia.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 16 citations in OpenAlex.
- Chemokine-Receptor Modulation Shapes Neuroinflammatory and Biomechanical Responses in Organotypic Hippocampal Cultures After Oxygen-Glucose Deprivation.ACS chemical neuroscience · 2026Article
- Electroacupuncture Preconditioning Ameliorates the Ischemic Microenvironment to Improve Long-Term Potentiation in Chronic Cerebral Hypoperfusion Rats With MGE Neural Progenitor Transplantation.Neural plasticity · 2025Article
- Fractalkine/CX3CR1 axis is critical for neuroprotection induced by hypoxic postconditioning against cerebral ischemic injury.Cell communication and signaling : CCS · 2024Article
- Succinum extracts inhibit microglial-derived neuroinflammation and depressive-like behaviors.Frontiers in pharmacology · 2022Article
- Microglia-mediated neuroinflammation and neuroplasticity after stroke.Frontiers in cellular neuroscience · 2022Review
- Differences in TNF‑α and TNF‑R1 expression in damaged neurons and activated astrocytes of the hippocampal CA1 region between young and adult gerbils following transient forebrain ischemia.Molecular medicine reports · 2021Article
- Orthopedic surgery-induced cognitive dysfunction is mediated by CX3CL1/R1 signaling.Journal of neuroinflammation · 2021Article
- CD200 Change Is Involved in Neuronal Death in Gerbil Hippocampal CA1 Field Following Transient Forebrain Ischemia and Postischemic Treatment with Risperidone Displays Neuroprotection without CD200 Change.International journal of molecular sciences · 2021Article
- Increased Calbindin D28k Expression via Long-Term Alternate-Day Fasting Does Not Protect against Ischemia-Reperfusion Injury: A Focus on Delayed Neuronal Death, Gliosis and Immunoglobulin G Leakage.International journal of molecular sciences · 2021Article
- Upregulation of Neuronal Cylindromatosis Expression is Essential for Electroacupuncture-Mediated Alleviation of Neuroinflammatory Injury by Regulating Microglial Polarization in Rats Subjected to Focal Cerebral Ischemia/Reperfusion.Journal of inflammation research · 2021Article
- Comparison of neuronal death and expression of TNF‑α and MCT4 in the gerbil hippocampal CA1 region induced by ischemia/reperfusion under hyperthermia to those under normothermia.Molecular medicine reports · 2020Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemokine C‑X3‑C motif ligand 1 (CX3CL1) and its sole receptor, CX3CR1, are known to be involved in neuronal damage/death following brain ischemia. In the present study, time‑dependent expression changes of CX3CL1 and CX3CR1 proteins were investigated in the hippocampal CA1 field following 5 min of transient global cerebral ischemia (tgCI) in gerbils. To induce tgCI in gerbils, bilateral common carotid arteries were occluded for 5 min using aneurysm clips. Expression changes of CX3CL1 and CX3CR1 proteins were assessed at 1, 2 and 5 days after tgCI using western blotting and immunohistochemistry. CX3CL1 immunoreactivity was strong in the CA1 pyramidal cells of animals in the sham operation group. Weak CX3CL1 immunoreactivity was detected at 6 h after tgCI, recovered at 1 day after tgCI and disappeared from 5 days after tgCI. CX3CR1 immunoreactivity was very weak in CA1 pyramidal cells of the sham animals. CX3CR1 immunoreactivity in CA1 pyramidal cells was significantly increased at 1 days after tgCI and gradually decreased thereafter. On the other hand, CX3CR1 immunoreactivity was significantly increased in microglia from 5 days after tgCI. These results showed that CX3CL1 and CX3CR1 protein expression levels in pyramidal cells and microglia in the hippocampal CA1 field following tgCI were changed, indicating that tgCI‑induced expression changes of CX3CL1 and CX3CR1 proteins might be closely associated with tgCI‑induced delayed neuronal death and microglial activation.
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