Complement-dependent P-selectin expression and injury following ischemic stroke.

Complement-dependent P-selectin expression and injury following ischemic stroke. Research Abstract Details 

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Complement-dependent P-selectin expression and injury following ischemic stroke. Abstract Text:

Carl Atkinson,Hong Zhu,Fei Qiao,Juan Carlos Varela,Jin Yu,Hongbin Song,Mark S Kindy,Stephen Tomlinson,

The mechanisms that contribute to inflammatory damage following ischemic stroke are poorly characterized, but studies indicate a role for both complement and P-selectin. In this study, we show that compared with wild-type mice, C3-deficient mice showed significant improvement in survival, neurological deficit, and infarct size at 24 h after middle cerebral artery occlusion and reperfusion. Furthermore, P-selectin protein expression was undetectable in the cerebral microvasculature of C3-deficient mice following reperfusion, and there was reduced neutrophil influx, reduced microthrombus formation, and increased blood flow postreperfusion in C3-deficient mice. We further investigated the use of a novel complement inhibitory protein in a therapeutic paradigm. Complement receptor 2 (CR2)-Crry inhibits complement activation at the C3 stage and targets to sites of complement activation. Treatment of normal mice with CR2-Crry at 30 min postreperfusion resulted in a similar level of protection to that seen in C3-deficient mice in all of the above-measured parameters. The data demonstrate an important role for complement in cerebrovascular thrombosis, inflammation, and injury following ischemic stroke. P-selectin expression in the cerebrovasculature, which is also implicated in cerebral ischemia and reperfusion injury, was shown to be distal to and dependent on complement activation. Data also show that a CR2-targeted approach of complement inhibition provides appropriate bioavailability in cerebral injury to enable complement inhibition at a dose that does not significantly affect systemic levels of serum complement activity, a potential benefit for stroke patients where immunosuppression would be undesirable due to significantly increased susceptibility to lung infection.

Complement-dependent P-selectin expression and injury following ischemic stroke. Publishing Authors By Initials

C Atkinson,H Zhu,F Qiao,JC Varela,J Yu,H Song,MS Kindy,S Tomlinson,

For similar investigative techniques: epidemiologic methods: statistics as topic: survival analysis research abstracts see: investigative techniques: epidemiologic methods: statistics as topic: survival analysis research

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Complement-dependent P-selectin expression and injury following ischemic stroke. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 177

Page Numbers: 7266-74

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 15

MONTH: Nov

YEAR: 2006

Complement-dependent P-selectin expression and injury following ischemic stroke. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Complement-dependent P-selectin expression and injury following ischemic stroke. Keywords Mesh Terms:

KEYWORDS: Survival Analysis

MESH TERMS: therapy

Chemical & Substance for Abstract: Complement-dependent P-selectin expression and injury following ischemic stroke. Information

Substance Name: Receptors, Complement 3d

Registry Number: 0

Grant and Affiliation Information for Complement-dependent P-selectin expression and injury following ischemic stroke.

AFFILIATION: Department of Microbiology and Immunology, Children's Research Institute, Medical University of South Carolina, Charleston, SC 29425, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL082485

ACRONYM: HL

MEDLINETA: J Immunol

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