ArticleActa pharmacologica Sinica2022
Neuronal chemokine-like-factor 1 (CKLF1) up-regulation promotes M1 polarization of microglia in rat brain after stroke.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 18 citations in OpenAlex.
- Dihydromyricetin Ameliorates Myocardial Ischemia-Reperfusion Injury by Modulating CKLF1-Mediated Cardiomyocyte Pyroptosis.Phytotherapy research : PTR · 2026Article
- Ginsenoside Rg1 alleviates post-ischemic stroke neuroinflammation by inhibiting CKLF1-mediated suppression of dead/dying neuron clearance.Acta pharmaceutica Sinica. B · 2026Article
- C-terminal Fragment Generated by HOIL-1 Cleavage Suppresses Inflammatory Responses of Myeloid Cells to Alleviate Colitis.Theranostics · 2026Article
- Cellular Communication Networks Mediated by Microglia in Ischemic Stroke.CNS neuroscience & therapeutics · 2025Review
- miR-21-5p Alleviates Retinal Ischemia-Reperfusion Injury by Inhibiting M1 Polarization of Microglia via Suppression of STAT3 Signaling.Biomedicines · 2025Article
- CKLF1 disrupts microglial efferocytosis following acute ischemic stroke by binding to phosphatidylserine.Cell death and differentiation · 2025Article
- Chemokines-like factor 1 as a serological biomarker in relation to disease severity and 90-day prognosis after spontaneous intracerebral hemorrhage: a prospective cohort study.Neurosurgical review · 2025Article
- Acupuncture Improves Chronic Cerebral Ischemia by Inhibiting the CKLF1/HIF-1α/VEGF/Notch1 Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
- Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders.Journal of neuroinflammation · 2025Review
- Examining the Impact of Microglia on Ischemic Stroke With an Emphasis on the Metabolism of Immune Cells.CNS neuroscience & therapeutics · 2025Review
- Ginsenoside Rg1 ameliorates stress-exacerbated Parkinson's disease in mice by eliminating RTP801 and α-synuclein autophagic degradation obstacle.Acta pharmacologica Sinica · 2025Article
- Microglia Autophagy Mediated by TMEM166 Promotes Ischemic Stroke Secondary to Carotid Artery Stenosis.Aging and disease · 2024Article
- Utility of serum chemokine-like factor 1 as a biomarker of severity and prognosis after severe traumatic brain injury: A prospective observational study.Brain and behavior · 2024Observational
- CKLF induces microglial activation via triggering defective mitophagy and mitochondrial dysfunction.Autophagy · 2024Article
- Regulation of oxygen-glucose deprivation/reperfusion-induced inflammatory responses and M1-M2 phenotype switch of BV2 microglia by lobetyolin.Metabolic brain disease · 2023Article
- A novel small-molecular CCR5 antagonist promotes neural repair after stroke.Acta pharmacologica Sinica · 2023Article
- A breakdown of metabolic reprogramming in microglia induced by CKLF1 exacerbates immune tolerance in ischemic stroke.Journal of neuroinflammation · 2023Article
- CZK, a novel alkaloid derivative from Clausena lansium, alleviates ischemic stroke injury through Nrf2-mediated antioxidant effects.Scientific reports · 2023Article
- Characterization of the Involvement of Tumour Necrosis Factor (TNF)-α-Stimulated Gene 6 (TSG-6) in Ischemic Brain Injury Caused by Middle Cerebral Artery Occlusion in Mouse.International journal of molecular sciences · 2023Article
- Tumor Necrosis Factor (TNF)-α-Stimulated Gene 6 (TSG-6): A Promising Immunomodulatory Target in Acute Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phenotypic transformation of microglia in the ischemic penumbra determines the outcomes of ischemic stroke. Our previous study has shown that chemokine-like-factor 1 (CKLF1) promotes M1-type polarization of microglia. In this study, we investigated the cellular source and transcriptional regulation of CKLF1, as well as the biological function of CKLF1 in ischemic penumbra of rat brain. We showed that CKLF1 was significantly up-regulated in cultured rat cortical neurons subjected to oxygen-glucose deprivation/reoxygenation (ODG/R) injury, but not in cultured rat microglia, astrocytes and oligodendrocytes. In a rat model of middle cerebral artery occlusion, we found that CKLF1 was up-regulated and co-localized with neurons in ischemic penumbra. Furthermore, the up-regulated CKLF1 was accompanied by the enhanced nuclear accumulation of NF-κB. The transcriptional activity of CKLF1 was improved by overexpression of NF-κB in HEK293T cells, whereas application of NF-κB inhibitor Bay 11-7082 (1 μM) abolished it, caused by OGD/R. By using chromatin-immunoprecipitation (ChIP) assay we demonstrated that NF-κB directly bound to the promoter of CKLF1 (at a binding site located at -249 bp to -239 bp of CKLF1 promoter region), and regulated the transcription of human CKLF1. Moreover, neuronal conditional medium collected after OGD/R injury or CKLF1-C27 (a peptide obtained from secreted CKLF1) induced the M1-type polarization of microglia, whereas the CKLF1-neutralizing antibody (αCKLF1) or NF-κB inhibitor Bay 11-7082 abolished the M1-type polarization of microglia. Specific knockout of neuronal CKLF1 in ischemic penumbra attenuated neuronal impairments and M1-type polarization of microglia caused by ischemic/reperfusion injury, evidenced by inhibited levels of M1 marker CD16/32 and increased expression of M2 marker CD206. Application of CKLF1-C27 (200 nM) promoted the phosphorylation of p38 and JNK in microglia, whereas specific depletion of neuronal CKLF1 in ischemic penumbra abolished ischemic/reperfusion-induced p38 and JNK phosphorylation. In summary, CKLF1 up-regulation in neurons regulated by NF-κB is one of the crucial mechanisms to promote M1-type polarization of microglia in ischemic penumbra.
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