Key result
Anti-P-selectin or anti-PSGL-1 therapy cuts post-injury neointima formation by ~65% in mice.
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BACKGROUND: Emerging data suggest that P-selectin, by controlling adhesion of white blood cells, may be important in limiting the response to vascular injury. METHODS AND RESULTS: We tested the hypothesis that transient inhibition of P-selectin with either anti-P-selectin monoclonal antibody (mAb) or anti-P-selectin glycoprotein ligand-1 (PSGL-1) mAb would reduce neointima formation in the setting of carotid denudation injury in atherosclerosis-prone apolipoprotein E-/- mice. Neointima formation at 28 days was reduced significantly, by 50% or 80%, by a single injection on the day of injury of 100 or 200 microg P-selectin mAb RB 40.34 and by 55% by a single injection of 100 microg PSGL-1 mAb 4RA10 (P< or =0.005). In addition, there was a significant reduction in neointimal macrophage content. CONCLUSIONS: These findings demonstrate that transient P-selectin or PSGL-1 blockade at the time of arterial injury significantly limits plaque macrophage content and neointima formation in a dose-dependent manner after carotid denudation injury in apolipoprotein E-/- mice.
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Phillips et al. (2003) studied Arterial injury / Atherosclerosis. Anti-P-selectin monoclonal antibody (mAb) or anti-PSGL-1 mAb was evaluated on Neointima formation at 28 days (50% to 80% reduction, p=<=0.005). A single injection of anti-P-selectin or anti-PSGL-1 monoclonal antibody reduced neointima formation by 50% to 80% after arterial injury in apolipoprotein E-deficient mice (P<=0.005).
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