The pituitary adenylate cyclase–activating polypeptide is a physiological inhibitor of platelet activation
J. Clin. Invest. Kathleen Freson, et al. 113:905 doi:10.1172/JCI19252 [
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Figure 4PACAP detection in fibroblasts and plasma. (A) Semiquantitative RT-PCR using 20 and 17 cycles showed PACAP(1–38) overexpression in fibroblasts from patient VI:1 compared with the control. RT-PCR was performed on two separate fibroblast samples, and β-actin is the internal control. (B) PACAP mRNA detection in fibroblasts, megakaryocytic cell lines DAMI, MEG-01, and K562, and platelets was performed by RT-PCR. (C) Immunoblot analysis of the VPAC1 receptor (58 kDa) in platelets from two unrelated controls and patient VI:1. (D) PACAP detections by ELISA in plasma from citrate (left panel) or ACD (right panel) blood from VI:1 (squares) and V:4 (triangles) or IV:5 (circles) and V:3 (filled diamonds) versus a citrated plasma pool (asterisks) or IV:6 (open diamonds). (E) The left panel shows the dose-dependent stimulation by PACAP(6–38) of the collagen-induced (0.2 μg/ml) aggregation of normal human platelets; representative tracings of five separate experiments are shown. The right panel illustrates the effect of PACAP(6–38) on collagen-induced (2 μg/ml) platelet aggregation in patient VI:1. Coll, collagen.
