Lack of platelet endothelial cell adhesion molecule-1 attenuates foreign body inflammation because of decreased angiogenesis

摘要: Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a 130-kd member of the immunoglobulin superfamily proteins, expressed on cells, leukocytes, and platelets. Antibody-blocking studies have implicated it in modulating leukocyte transmigration angiogenesis. However, generation PECAM-1 knockout mouse has shown that its function can be compensated for by similarly acting proteins because most acute inflammatory models proceed comparable manner wild-type animals. We decided to examine chronic process foreign body inflammation. show PECAM-1-deficient mice exhibit attenuated neutrophil infiltration around subcutaneous polyvinyl acetyl implant. Bone marrow engraftment indicate lack CD31 expression endothelium determines diminished accumulation implants. Specifically, we find decreased angiogenesis (as manifested lower vessel density, hemoglobin content, less laminin deposition) correlates with This study indicates absence results therefore delivery leukocytes