The contributions of platelet and endothelial cell PECAM-1 to the regulation of thrombus formation. (A) Chimeric mice were generated by bone marrow transplantation and, following recovery, successful engraftment was verified by flow cytometric analysis to detect the presence or absence of PECAM-1 on lymphocytes from WT mice that received transplants of WT bone marrow (Ai), WT mice that received transplants of PECAM-1–deficient bone marrow (Aii), and PECAM-1–deficient mice that received transplants of WT bone marrow (Aiii). (B) Median anti-CD41 integrated fluorescence (Bi) and thrombus area (μm²) (Bii) were calculated for thrombi formed in chimeric mice generated by bone marrow transplantation and are plotted against time for a duration of 120 seconds following thrombus initiation (Bi: WT mice with WT BM: n = 30, PECAM-1–deficient mice with WT bone marrow: n = 33, WT mice with PECAM-1–deficient bone marrow: n = 14; ii: WT mice with WT BM: n = 26, PECAM-1–deficient mice with WT bone marrow: n = 33, WT mice with PECAM-1–deficient bone marrow: n = 14). KO indicates knock-out. (C) Fibrin deposition in thrombi was measured simultaneously with platelet accumulation for each type of mouse chimera that received transplants and is plotted against time for the duration of 120 seconds following thrombus initiation (WT mice with WT BM: n = 30; PECAM-1–deficient mice with WT bone marrow: n = 32; WT mice with PECAM-1–deficient bone marrow: n = 14).