Novel molecules in calcium signaling in platelets.
A rise in the intracellular calcium (Ca2+) concentration is a major component of the signaling mechanisms regulating platelet function in thrombosis and hemostasis. Previous studies, however, failed to identify many key molecules regulating Ca2+ signaling in platelets. Here, we review recent findings, which identified CalDAG-GEFI as a critical Ca2+ sensor that links increases in intracellular Ca2+ to integrin activation, TxA2 formation, and granule release in stimulated platelets. Furthermore, we summarize work that lead to the discovery of STIM1 and Orai1 as key regulators of store-operated calcium entry (SOCE) in platelets. A short discussion on the usefulness of each molecule as a potential new target for antiplatelet therapy is included.
Bergmeier
W
W
Cardeza Foundation and Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA. wolfgang.bergmeier@jefferson.edu
Stefanini
L
L
D001792:Blood Platelets / Q000378:metabolism*; D015220:Calcium Channels; D020013:Calcium Signaling; D006801:Humans; D008565:Membrane Proteins; D009363:Neoplasm Proteins; D000071740:ORAI1 Protein; D010975:Platelet Aggregation Inhibitors; D000071737:Stromal Interaction Molecule 1
D015220:Calcium Channels; D008565:Membrane Proteins; D009363:Neoplasm Proteins; D000071740:ORAI1 Protein; C510746:ORAI1 protein, human; D010975:Platelet Aggregation Inhibitors; C103530:STIM1 protein, human; D000071737:Stromal Interaction Molecule 1