Journal
LIFE SCIENCES
Volume 78, Issue 26, Pages 2983-2988Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2005.11.027
Keywords
brain microvascular endothelial cells; C-reactive protein; cell adhesion molecules; lactate dehydrogenase
Ask authors/readers for more resources
Ischemic stroke can trigger an acute phase response resulting in a rise of plasma concentration of C-reactive protein (CRP). Clinical data about the relationship between CRP and prognosis suggest that CRP might be involved in the pathogenesis of cerebral ischemia. In the present work, a significant increase of circulating level of CRP was observed in an vivo rat brain ischemia model of middle cerebral artery occlusion. To determine the possible effects of CRP on brain microvessel endothelium, we performed a dose-dependent experiment in mouse brain microvascular endothelial cells (bEnd.3 cells) with emphasis on its relation to cell adhesions molecules. Incubation with CRP (1-75 mg/L) for 24 It significantly increased Lactate dehydrogenase (LDH) leakage from bEnd.3 cells (P < 0.01) in a dose-dependent manner, and induced significant up-reglations of intercellular adhesion molecule-1 (VCAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions analyzed P by Western blotting (P < 0.01). In contrast to earlier report, CRP also induced significant increase in ICAM-1 expression in the absence of serum (P < 0.01). In conclusion, the present results suggest that CRP may be involved directly in the development of inflammation in response to cerebral ischemia. (c) 2005 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available