Disease relevance of SELP

• Effects of a monoclonal antibody to P-selectin on recovery of neonatal lamb hearts after cold cardioplegic ischemia [1].
• Blocking P-selectin in vivo with a functionally inhibitory antibody prevented development of proteinuria and skin swelling following antigen challenge [2].
• The role of P-selectin in T-lymphocyte accumulation and injury was studied in delayed-type hypersensitivity (DTH) responses in the skin and glomeruli of rats [2].
• P-selectin directs T lymphocyte-mediated injury in delayed-type hypersensitivity responses: studies in glomerulonephritis and cutaneous delayed-type hypersensitivity [2].
• P-selectin blockade fails to improve acute lung injury in sheep [3].

High impact information on SELP

• Strategies to block P-selectin mediated neutrophil adherence may have clinical application in improving myocardial function at early reperfusion [1].
• P-selectin, which is expressed on activated endothelium, mediates the first step in leukocyte adherence to the endothelium [1].
• Macrophage and intrinsic glomerular cell proliferation were reduced at both doses of IL-10, as was glomerular expression of P-selectin and monocyte chemoattractant protein-1 [4].
• Up-regulation of P-selectin expression on endothelial cells was observed in both inflammatory lesions [2].
• These results suggest that endogenous GC modulate heterologous anti-GBM nephritis in rats and that this may be attributable, in part, to regulation of P-selectin expression [5].

Anatomical context of SELP

• Local accumulation of T cells and macrophages was markedly attenuated in glomeruli and the skin and up-regulation of endothelial cell P-selectin was prevented [2].

Analytical, diagnostic and therapeutic context of SELP

• Immediately before reperfusion, mAb to P-selectin was administered to the perfusate (15 micrograms/mL) in 6 hearts (group P-sel) [1].

References