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Title

Anti-VCAM-1 antibodies did not protect against ischemic damage either in rats or in mice

AuthorsJusticia, Carles ; Martín, Abraham; Rojas, Santiago ; Gironella, Meritxell; Cervera, Álvaro; Panés, Julián; Chamorro, Ángel; Planas, Anna M.
KeywordsRemote organs
Rodents
Middle cerebral artery occlusion
Leukocytes
Antibody treatment
Adhesion molecules
Issue Date3-Aug-2005
PublisherLippincott Williams & Wilkins
CitationJournal of Cerebral Blood Flow and Metabolism 26(3): 421-432 (2006)
AbstractCerebral ischemia triggers an inflammatory process involving the infiltration of leukocytes to the parenchyma. Circulating leukocytes adhere to the vascular wall through adhesion molecules. Here we quantified the in vivo expression of vascular cell adhesion molecule-1 (VCAM-1) in the brain, heart and lungs from 6 to 48 h after transient middle cerebral artery (MCA) occlusion in rats, by intravenous injection of a tracer radiolabelled anti-VCAM-1 antibody. The vascular localization of VCAM-1 was verified by immunohistochemistry after in vivo injection of the antibody. Vascular cell adhesion molecule-1 was strongly induced (4-fold at 24 h) in the microvasculature of the ischemic area, and, to a lesser extent, in the contralateral hemisphere and in a remote organ, the heart, but not in the lungs, indicating that the inflammatory process propagates beyond the injured brain. We injected intravenously either blocking doses of anti-VCAM-1 antibodies or control antibodies after MCA occlusion in rats and mice. We evaluated the neurological score in rats, and infarct volume at 2 days in rats and at 4 days in mice. Anti-VCAM-1 did not protect against ischemic damage either in rats or in mice. Vascular cell adhesion molecule-1 blockade significantly decreased the number of ED1 (labeling monocytes /macrophages/reactive microglia)-positive cells in the ischemic rat brain. However, it did not reduce the numbers of infiltrating neutrophils and lymphocytes, and total leukocytes (CD45 positive), which showed a trend to increase. The results show vascular upregulation of VCAM-1 after transient focal ischemia, but no benefits of blocking VCAM-1, suggesting that this is not a therapeutical strategy for stroke treatment. © 2006 ISCBFM All rights reserved.
Publisher version (URL)http://dx.doi.org/10.1038/sj.jcbfm.9600198
URIhttp://hdl.handle.net/10261/116637
DOI10.1038/sj.jcbfm.9600198
Identifiersdoi: 10.1038/sj.jcbfm.9600198
issn: 0271-678X
Appears in Collections:(IIBB) Artículos
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