Novel whole blood assay for phenotyping platelet reactivity in mice identifies ICAM-1 as a mediator of platelet-monocyte interaction.

摘要: Testing of platelet function is central to the cardiovascular phenotyping genetically modified mice. Traditional tests have been developed primarily for testing human samples and volumes required make them highly unsuitable mouse platelets. This limits research in this area. To address problem, we a miniaturized whole blood aggregometry assay, based on readily accessible 96-well plate format coupled with quantification single depletion by flow cytometric analysis. Using approach, observed concentration-dependent loss platelets exposed arachidonic acid, collagen, U46619 or protease activated receptor 4 activating peptide. was sensitive well-established antiplatelet agents genetic manipulation activation pathways. Observations were more deeply analyzed imaging, confocal measurement releasates. Phenotypic analysis reactivity taken from mice lacking intercellular adhesion molecule (ICAM)-1 identified marked decrease fibrinogen-dependent platelet-monocyte interactions, especially under inflammatory conditions. Such findings exemplify value screening phenotypes shed further light upon roles interactions inflammation.