ArticleJournal of cerebrovascular and endovascular neurosurgery2021
Systemic macrophage depletion attenuates infarct size in an experimental mouse model of stroke.
Article in Journal of cerebrovascular and endovascular neurosurgery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Meis1-driven suppression of MIF/CD74 signaling promotes M2 macrophage polarization and protects against inflammatory damage in experimental acute lung injury.Cell biology and toxicology · 2026Article
- Effects of peripheral blood cells on ischemic stroke: Greater immune response or systemic inflammation?Heliyon · 2024Review
- Article
- Inflammatory Responses After Ischemic Stroke.Seminars in immunopathology · 2022Review
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Authors and funding
6 authors.
Funding
Abstract
objectiveMacrophages have been shown to play important roles in various pathophysiological processes of the central nervous system via neuroinflammation, leading to an increased interest in macrophage biology. Circulating blood monocytes are among the first cells to infiltrate the brain after ischemic stroke; however, the role of innate immune cells such as monocytes and macrophages remains to be elucidated. Here, we investigated the association between blood monocytes and infarct size following ischemic stroke.
methodsWe induced stroke using a focal ischemia mouse model through middle cerebral artery suture occlusion. To deplete circulating blood monocytes, clodronate was injected intraperitoneally 24 h before the surgery. Animals were sacrificed at specified time points, and the infarct size and mRNA expression were then measured.
resultsThe clodronate-injected mice showed significantly smaller infarct size than the control mice. Immunohistochemical staining revealed that monocyte depletion significantly blocked the infiltration of macrophages and microglia. The mRNA expression levels of macrophage and microglia markers were higher in the left infarcted brain than in the right non-infarcted brain.
conclusionsIn summary, monocyte depletion reduced the infarct size and mitigated neurological deficits in mice following ischemic stroke, likely by blocking the infiltration of inflammatory cells such as macrophages and microglia.
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