ArticleJournal of neuroinflammation2020
Rh-CSF1 attenuates neuroinflammation via the CSF1R/PLCG2/PKCε pathway in a rat model of neonatal HIE.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- Hypoxic-Ischemic Encephalopathy: Pathogenesis and Promising Therapies.Molecular neurobiology · 2025Pooled it
- A systematic review of immune-based interventions for perinatal neuroprotection: closing the gap between animal studies and human trials.Journal of neuroinflammation · 2023Pooled it
- Intranasal therapies for neonatal hypoxic-ischemic encephalopathy.Neural regeneration research · 2026Article
- Sex-specific effects of therapeutic hypothermia on short- and long-term microglial and astrocytic reactivity after severe neonatal hypoxia-ischemia.Metabolic brain disease · 2026Article
- Inhibition of PKCγ phosphorylation protects against cerebral ischemia-reperfusion injury.Redox biology · 2026Article
- Toward Early Diagnosis and Therapeutic Discovery in CLN3 Disease: A Computational Biomarker Discovery Framework.medRxiv : the preprint server for health sciences · 2026Article
- Anti-inflammatory mechanisms ofInternational journal of ophthalmology · 2026Article
- The umbilical cord blood exosome MFG-E8 alleviates hypoxic-ischemic encephalopathy brain injury in neonatal rats by restoring autophagy flux and inhibiting ferroptosis through GSK3β/β-catenin signaling.Regenerative therapy · 2025Article
- TREM2 Modulates Postoperative Cognitive Function in Aged Mice by Inhibiting the NLRP3/caspase-1 Pathway and Apoptosis via PLCγ2 Activation.Molecular neurobiology · 2025Article
- PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Ptprz Signaling, Tubule-Mediated and Macrophage-Mediated Kidney Injury, and Subsequent CKD.Journal of the American Society of Nephrology : JASN · 2025Article
- The role of the sensory input intervention in recovery of the motor function in hypoxic ischemic encephalopathy rat model.Journal of neurophysiology · 2024Article
- Inflammatory and Hematologic Liver and Platelet (HALP) Scores in Hypothermia-Treated Hypoxic-Ischemic Encephalopathy (HIE).Children (Basel, Switzerland) · 2024Article
- Cerebrospinal fluid exploratory proteomics and ketamine metabolite pharmacokinetics in human volunteers after ketamine infusion.iScience · 2023Article
- Paeonol protects against doxorubicin-induced cardiotoxicity by promoting Mfn2-mediated mitochondrial fusion through activating the PKCε-Stat3 pathway.Journal of advanced research · 2023Article
- Microglia dynamic response and phenotype heterogeneity in neural regeneration following hypoxic-ischemic brain injury.Frontiers in immunology · 2023Review
- Persistent cortical and white matter inflammation after therapeutic hypothermia for ischemia in near-term fetal sheep.Journal of neuroinflammation · 2022Article
- Colony stimulating factor 1: friend or foe of neurons?Neural regeneration research · 2022Article
- Integrative analysis of DNA methylation and gene expression reveals key molecular signatures in acute myocardial infarction.Clinical epigenetics · 2022Article
- PLCγ2 impacts microglia-related effectors revealing variants and pathways important in Alzheimer's disease.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundHypoxic-ischemic encephalopathy (HIE) is a life-threatening cerebrovascular disease. Neuroinflammation plays an important role in the pathogenesis of HIE, in which microglia are key cellular mediators in the regulation of neuroinflammatory processes. Colony-stimulating factor 1 (CSF1), a specific endogenous ligand of CSF1 receptor (CSF1R), is crucial in microglial growth, differentiation, and proliferation. Recent studies showed that the activation of CSF1R with CSF1 exerted anti-inflammatory effects in a variety of nervous system diseases. This study aimed to investigate the anti-inflammatory effects of recombinant human CSF1 (rh-CSF1) and the underlying mechanisms in a rat model of HIE.
methodsA total of 202 10-day old Sprague Dawley rat pups were used. HI was induced by the right common carotid artery ligation with subsequent exposure of 2.5-h hypoxia. At 1 h and 24 h after HI induction, exogenous rh-CSF1 was administered intranasally. To explore the underlying mechanism, CSF1R inhibitor, BLZ945, and phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, were injected intraperitoneally at 1 h before HI induction, respectively. Brain infarct area, brain water content, neurobehavioral tests, western blot, and immunofluorescence staining were performed.
resultsThe expressions of endogenous CSF1, CSF1R, PLCG2, protein kinase C epsilon type (PKCε), and cAMP response element-binding protein (CREB) were gradually increased after HIE. Rh-CSF1 significantly improved the neurological deficits at 48 h and 4 weeks after HI, which was accompanied by a reduction in the brain infarct area, brain edema, brain atrophy, and neuroinflammation. Moreover, activation of CSF1R by rh-CSF1 significantly increased the expressions of p-PLCG2, p-PKCε, and p-CREB, but inhibited the activation of neutrophil infiltration, and downregulated the expressions of IL-1β and TNF-α. Inhibition of CSF1R and PLCG2 abolished these neuroprotective effects of rh-CSF1 after HI.
conclusionsOur findings demonstrated that the activation of CSF1R by rh-CSF1 attenuated neuroinflammation and improved neurological deficits after HI. The anti-inflammatory effects of rh-CSF1 partially acted through activating the CSF1R/PLCG2/PKCε/CREB signaling pathway after HI. These results suggest that rh-CSF1 may serve as a potential therapeutic approach to ameliorate injury in HIE patients.
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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.