ArticleJournal of neuroinflammation2022
Scavenger receptor CD36 governs recruitment of myeloid cells to the blood-CSF barrier after stroke in neonatal mice.
Article in Journal of neuroinflammation, 2022. 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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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Multifaceted Immune Effects of the Scavenger Receptor CD36 on Long-Term Outcomes After Neonatal Arterial Focal Stroke.Journal of neurochemistry · 2026Article
- CD36-mediated lipid-accumulation in reactive microglia contributes to retinal degeneration via the NLRP3-IL-1β pathway in mice.Nature communications · 2026Article
- Progranulin haploinsufficiency remodels the cerebral microvasculature and neurovascular unit.bioRxiv : the preprint server for biology · 2026Article
- CD36-PPARγ-SPP1 axis mediates hepatocyte-macrophage coordination to drive MASLD-related liver fibrosis.JHEP reports : innovation in hepatology · 2026Article
- Adenosine AJournal of the American Heart Association · 2025Article
- Immune genes involved in synaptic plasticity during early postnatal brain development contribute to post-stroke damage in the aging male rat brain.Biogerontology · 2025Article
- Brain Maturation as a Fundamental Factor in Immune-Neurovascular Interactions in Stroke.Translational stroke research · 2024Review
- Immune-Neurovascular Interactions in Experimental Perinatal and Childhood Arterial Ischemic Stroke.Stroke · 2024Review
- Monocyte-related cytokines/chemokines in cerebral ischemic stroke.CNS neuroscience & therapeutics · 2023Review
- Monocytes in neonatal stroke and hypoxic-ischemic encephalopathy: Pathophysiological mechanisms and therapeutic possibilities.Neuroprotection (Chichester, England) · 2023Review
- Immune compartments at the brain's borders in health and neurovascular diseases.Seminars in immunopathology · 2023Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundIschemic stroke induces the activation and recruitment of peripheral leukocytes to the injured brain. These cells can infiltrate the brain through multiple routes, either by penetrating blood-brain barrier or via blood-CSF barriers at the meninges or the choroid plexus (CP). We previously showed that myeloid cell trafficking via the CP occurs early after neonatal arterial stroke and modulates injury. CD36 is a receptor that mediates function of endothelial cells and cells of the monocyte lineage under various neurodegenerative conditions and can influence brain injury after neonatal stroke. Here we asked whether CD36 impacts injury by altering leukocyte trafficking through the CP in neonatal mice subjected to transient middle cerebral artery occlusion (tMCAO).
methodsIn neonatal mice with intact or globally disrupted CD36 signalling (CD36 KO), we characterized the phenotypes of myeloid cells by flow cytometry and the underlying gene expression signatures in the CPs contralateral and ipsilateral to tMCAO by RNA sequencing analyses, focussing on early post-reperfusion time window.
resultsFlow cytometry in the isolated CPs revealed that CD36 mediates stepwise recruitment of myeloid cells to the CP ipsilateral to tMCAO early after reperfusion, with a predominant increase first in inflammatory monocyte subsets and neutrophils followed by patrolling monocytes. RNA sequencing analyses demonstrated marked changes in gene expression in the CP ipsilateral compared to the CP contralateral to tMCAO in wild type mice. Changes were further modified by lack of CD36, including distinction in several clusters of genes involved in inflammatory, metabolic and extracellular matrix signalling in the CP ipsilateral to tMCAO.
conclusionAltogether, our data suggest cooperation between blood-CSF-brain interface via the CP through CD36-mediated signalling following neonatal stroke with a key role for inflammatory monocytes and neutrophils.
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