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Am J Physiol Heart Circ Physiol (August 12, 2004). doi:10.1152/ajpheart.00588.2004
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Submitted on June 14, 2004
Accepted on August 9, 2004

Contributions of leukocyte LFA-1 and Mac-1 to brain injury and microvascular dysfunction induced by transient middle cerebral artery occlusion

Thiruma V Arumugam1, James W Salter1, John H Chidlow1, Christie M Ballantyne1, Christopher G Kevil1, and D. Neil Granger1*

1 Department of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA

* To whom correspondence should be addressed. E-mail: dgrang{at}lsuhsc.edu.

While the {beta}2-integrins have been implicated in the pathogenesis of cerebral ischemia/reperfusion (I/R) injury, the relative contributions of the {alpha}-subunits to the pathogenesis of ischemic stroke remains unclear. The objective of this study was to determine if and how genetic deficiency of either LFA-1 or Mac-1 alters the blood cell-endothelial cell interactions, tissue injury and organ dysfunction in mouse brain exposed to focal I/R. Middle cerebral artery occlusion was induced for 1 hour (followed by either 4 or 24 hours of reperfusion) in wild type mice and in mice with null mutations for either LFA-1 or Mac-1. Neurological deficit and infarct volume were monitored 24 hours after reperfusion. Platelet- and leukocyte-vessel wall adhesive interactions were monitored in cortical venules by intravital microscopy. Mice with null mutations for LFA-1 or Mac-1 exhibited significant reductions in infarct volume. This was associated with a significant improvement in the I/R-induced neurological deficit. Leukocyte adhesion in cerebral venules did not differ between wild type and mutant mice at 4 hours after reperfusion. However, after 24 hours of reperfusion leukocyte adhesion was reduced in both LFA-1 and Mac-1 deficient mice, compared to their wild type counterparts. Platelet adhesion was also reduced at both 4 and 24 hours after reperfusion in the LFA-1 and Mac-1 deficient mice. These findings indicate that both {alpha} subunits of the {beta}2-integrins contribute to the brain injury, and blood cell-vessel wall interactions that are associated with transient focal cerebral ischemia.




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