Protein Kinase C isoforms (PKCs) are serine/threonine kinases that mediate multiple cellular functions and have been implicated in the patho-physiology of cancer, diabetes and cardiovascular diseases such as ischemia, cardiac hypertrophy, heart failure, and atherosclerosis. Blood components such as platelets contribute to thrombus formation resulting in stroke and myocardial infarction under patho-physiological conditions. PKCs mediate distinct platelet functional responses upon stimulation of different platelet receptors. Current research strategies employ the usage of PKC isoform-specific inhibitors to dissect their role in mediating platelet functional responses. This strategy has been complemented with studies in murine platelets lacking a specific PKC isoform. Furthermore, these studies have been extended to in vivo thrombosis animal models in order to correlate the in vitro observations to the formation of thrombus in vivo. It has been shown that PKCs play an important role in platelet secretion, aggregation and thrombus stabilization. In the current review, we discuss the role of various classes of PKCs in the complexity of signaling interplay in platelets, their implications to thrombosis, and also outline the possible therapeutic interventions.
Keywords: Protein Kinase C, thrombosis, Glycoprotein, Thromboxane A2, G-protein Coupled Receptor, Protease Activated Receptors, Phospholipase C, Diacylglyveral, Receptors for Activated C Kinase, Substrates that interact with C-Kinase, Phosphatidylinositol dependent Kinase-1, platelet exocytosis, Soluble N-ethylmaleimide, –, sensitive factor attachment protein receptors, SNare Attachment Protein, Vesicle Associated Membrane Protein, myristoylated alanine-rich C-kinase substrate, platelet and leukocyte C kinase substrate, Phorbol Myristic Acid, 1,2-dioctanoylglycerol, Ca+2 and DAG-regulated guanine nucleotide exchange factor I, ST segment elevation myocardial infarction, Percutaneous Coronary Intervention, platelets, Signaling, inhibitors