ArticleBiological research for nursing2011
Systemic neutrophil activation in a mouse model of ischemic stroke and reperfusion.
Article in Biological research for nursing, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- The role of efferocytosis in ischemic stroke and insights from retinopathy.Trends in neurosciences · 2025Review
- Implication of Hypotension in the Pathogenesis of Cognitive Impairment and Brain Injury in Chronic Liver Disease.Neurochemical research · 2024Review
- Hypothermic treatment reduces matrix metalloproteinase-9 expression and damage in the liver following asphyxial cardiac arrest in rats.Laboratory animal research · 2021Article
- Can quantifying morphology and TMEM119 expression distinguish between microglia and infiltrating macrophages after ischemic stroke and reperfusion in male and female mice?Journal of neuroinflammation · 2021Article
- Myosin1f-mediated neutrophil migration contributes to acute neuroinflammation and brain injury after stroke in mice.Journal of neuroinflammation · 2019Article
- Thrombosis, Neuroinflammation, and Poststroke Infection: The Multifaceted Role of Neutrophils in Stroke.Journal of immunology research · 2017Review
- Article
- Ischemia, Immunosuppression and Infection--Tackling the Predicaments of Post-Stroke Complications.International journal of molecular sciences · 2016Review
- Neonatal brain injury and systemic inflammation: modulation by activated protein C ex vivo.Clinical and experimental immunology · 2015Article
- The Yin and Yang of innate immunity in stroke.BioMed research international · 2014Review
- Curcuminoids limit neutrophil-mediated reperfusion injury in experimental stroke by targeting the endothelium.Microcirculation (New York, N.Y. : 1994) · 2013Article
- A quantitative spatiotemporal analysis of microglia morphology during ischemic stroke and reperfusion.Journal of neuroinflammation · 2013Article
- Astragalus Polysaccharide Suppresses the Expression of Adhesion Molecules through the Regulation of the p38 MAPK Signaling Pathway in Human Cardiac Microvascular Endothelial Cells after Ischemia-Reperfusion Injury.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Post-ischemic vascular adhesion protein-1 inhibition provides neuroprotection in a rat temporary middle cerebral artery occlusion model.Journal of neurochemistry · 2012Article
- AQP4 knockout aggravates ischemia/reperfusion injury in mice.CNS neuroscience & therapeutics · 2012Article
- Exaggerated neutrophil-mediated reperfusion injury after ischemic stroke in a rodent model of type 2 diabetes.Microcirculation (New York, N.Y. : 1994) · 2011Article
- Immunological methods for nursing research: from cells to systems.Biological research for nursing · 2011Review
- The contribution of mannose binding lectin to reperfusion injury after ischemic stroke.Current neurovascular research · 2011Article
- Anti-Inflammation of Natural Components from Medicinal Plants at Low Concentrations in Brain via Inhibiting Neutrophil Infiltration after Stroke.Mediators of inflammationReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
As a natural response to injury and disease, neutrophils activate, adhere to the microvasculature, migrate into brain tissue, and release toxic substances such as reactive oxygen species and proteases. This neutrophil response occurs when blood flow is returned to brain tissue (reperfusion) after ischemic stroke. Thus, the presence of activated systemic neutrophils increases the potential for tissue injury during reperfusion after ischemic stroke. Although experiments in rat models suggest that activated neutrophils play a pivotal role in cerebral ischemia reperfusion injury, little is known about systemic neutrophil activation during reperfusion following ischemic stroke in a mouse model. The purpose of this study was to characterize systemic leukocyte responses and neutrophil CD11b expression 15-min and 24-hr post-reperfusion in a mouse model of ischemic stroke. The intraluminal filament method of transient middle cerebral artery occlusion (tMCAO) with reperfusion or a sham procedure was performed in male C57Bl/6 mice. Automated leukocyte counts and manual white blood cell (WBC) differential counts were measured. Flow cytometry was used to assess systemic neutrophil surface CD11b expression. The data suggest that the damaging potential of systemic neutrophil activation begins as early as 15 min and remains evident at 24 hr after the initiation of reperfusion. In addition, because transgenic mouse models, bred on a C57Bl/6 background, are increasingly used to elucidate single mechanisms of reperfusion injury after ischemic stroke, findings from this study are foundational for future investigations examining the damaging potential of neutrophil responses post-reperfusion after ischemic stroke in genetically altered mouse models within this background strain.
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