ArticleCurrent neurovascular research2011
The contribution of mannose binding lectin to reperfusion injury after ischemic stroke.
Article in Current neurovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- PACAP glycosides promote cell outgrowth in vitro and reduce infarct size after stroke in a preclinical model.Neuroscience letters · 2024Article
- Insight into the Neuroprotective Effect of Genistein-3'-Sodium Sulfonate Against Neonatal Hypoxic-Ischaemic Brain Injury in Rats by Bioinformatics.Molecular neurobiology · 2023Article
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Complement Initiation Varies by Sex in Intestinal Ischemia Reperfusion Injury.Frontiers in immunology · 2021Article
- Inhibition of Complement Drives Increase in Early Growth Response Proteins and Neuroprotection Mediated by Salidroside After Cerebral Ischemia.Inflammation · 2018Article
- Roles of Specialized Pro-Resolving Lipid Mediators in Cerebral Ischemia Reperfusion Injury.Frontiers in neurology · 2018Review
- Microglial Lectins in Health and Neurological Diseases.Frontiers in molecular neuroscience · 2018Review
- Injury site-specific targeting of complement inhibitors for treating stroke.Immunological reviews · 2016Review
- Modulation of post-stroke degenerative and regenerative processes and subacute protection by site-targeted inhibition of the alternative pathway of complement.Journal of neuroinflammation · 2015Article
- TLR2 modulates antibodies required for intestinal ischemia/reperfusion-induced damage and inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Complement in the Homeostatic and Ischemic Brain.Frontiers in immunology · 2015Review
- Mannan-Binding Lectin Is Involved in the Protection against Renal Ischemia/Reperfusion Injury by Dietary Restriction.PloS one · 2015Article
- Mannan-binding lectin in cardiovascular disease.BioMed research international · 2014Review
- The alternative complement pathway propagates inflammation and injury in murine ischemic stroke.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Complement activation in the injured central nervous system: another dual-edged sword?Journal of neuroinflammation · 2012Review
- Pathogenic natural antibodies propagate cerebral injury following ischemic stroke in mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- The Neuroprotective Effect of Genetic Mannose-binding Lectin Deficiency is not Sustained in the Sub-acute Phase of Stroke.Translational stroke research · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
After complement system (CS) activation, the sequential production of complement products increases cell injury and death through opsonophagocytosis, cytolysis, adaptive, and inflammatory cell responses. These responses potentiate cerebral ischemia-reperfusion (IR) injury after ischemic stroke and reperfusion. Activation of the CS via mannose binding lectin (MBL)-initiated lectin pathway is known to increase tissue damage in response to IR in muscle, myocardium and intestine tissue. In contrast, the contribution of this pathway to cerebral IR injury, a neutrophil-mediated event, is less clear. Therefore, we investigated the potential protective role of MBL deficiency in neutrophil-mediated cerebral injury after IR. Using an intraluminal filament method, neutrophil activation and cerebral injury were compared between MBL-deficient and wild type C57Bl/6 mice subjected to 60 minutes of MCA ischemia and reperfusion. Systemic neutrophil activation was not decreased in MBL-deficient animals after IR. In MBL-deficient animals, cerebral injury was significantly decreased only in the striatum (p < 0.05). Despite MBL deficiency, C3 depositions were evident in the injured hemisphere during reperfusion. These results indicate that while MBL deficiency results in a modest protection of a sub-cortical brain region during IR, redundant complement pathway activation may overwhelm further beneficial effects of MBL deficiency during reperfusion.
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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.