2024-03-28T19:35:55Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1166372016-02-18T03:14:00Zcom_10261_105com_10261_1col_10261_358
2015-06-16T10:02:05Z
urn:hdl:10261/116637
Anti-VCAM-1 antibodies did not protect against ischemic damage either in rats or in mice
Justicia, Carles
Martín, Abraham
Rojas, Santiago
Gironella, Meritxell
Cervera, Álvaro
Panés, Julián
Chamorro, Ángel
Planas, Anna M.
Remote organs
Rodents
Middle cerebral artery occlusion
Leukocytes
Antibody treatment
Adhesion molecules
Cerebral 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.
2015-06-16T10:02:05Z
2015-06-16T10:02:05Z
2005-08-03
2015-06-16T10:02:06Z
artículo
Journal of Cerebral Blood Flow and Metabolism 26(3): 421-432 (2006)
http://hdl.handle.net/10261/116637
10.1038/sj.jcbfm.9600198
eng
http://dx.doi.org/10.1038/sj.jcbfm.9600198
closedAccess
Lippincott Williams & Wilkins