Abstract | BACKGROUND:
Ischemic stroke causes a strong inflammatory response that includes T cells, monocytes/macrophages, and neutrophils. Interaction of these immune cells with platelets and endothelial cells facilitates microvascular dysfunction and leads to secondary infarct growth. We recently showed that blocking of platelet glycoprotein (GP) receptor Ib improves stroke outcome without increasing the risk of intracerebral hemorrhage. Until now, it has been unclear whether GPIb only mediates thrombus formation or also contributes to the pathophysiology of local inflammation. METHODS: RESULTS: Blocking of GPIb reduced stroke size and improved functional outcome on day 1 after tMCAO without increasing the risk of intracerebral hemorrhage. As expected, disruption of GPIb-mediated pathways in platelets significantly reduced thrombus burden in the cerebral microvasculature. In addition, inhibition of GPIb limited the local inflammatory response in the ischemic brain as indicated by lower numbers of infiltrating T cells and macrophages and lower expression levels of inflammatory cytokines compared with rat IgG Fab-treated controls. CONCLUSION:
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Authors | Michael K Schuhmann, Josua Guthmann, Guido Stoll, Bernhard Nieswandt, Peter Kraft, Christoph Kleinschnitz |
Journal | Journal of neuroinflammation
(J Neuroinflammation)
Vol. 14
Issue 1
Pg. 18
(01 21 2017)
ISSN: 1742-2094 [Electronic] England |
PMID | 28109273
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Platelet Glycoprotein GPIb-IX Complex
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Topics |
- Animals
- Inflammation
(pathology)
- Male
- Mice
- Mice, Inbred C57BL
- Platelet Glycoprotein GPIb-IX Complex
(metabolism)
- Stroke
(metabolism, pathology)
- Thrombosis
(pathology)
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