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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Antineoplastic Agents, Apoptosis, Apoptosis Regulatory Proteins, Blood Platelets, Dose-Response Relationship, Drug, Enzyme Activation, Humans, Membrane Potential, Mitochondrial, Mitochondrial Membranes, Phosphorylation, Protein Kinase Inhibitors, Signal Transduction, Staurosporine, p38 Mitogen-Activated Protein Kinases.
user
Does staurosporine induce Platelet Apoptosis Through p38 Mitogen-Activated Protein Kinase Signaling Pathway? Context: Staurosporine (STS), a microbial alkaloid and potent PKC inhibitor, has become one of the most promising anti-cancer drugs. STS effectively induces apoptosis in many nucleated cells; however, it is still unclear whether STS induces apoptosis in enucleated platelets. Apoptotic events in platelets treated with STS were assessed by flow cytometry or western blotting. STS induced depolarization of mitochondrial inner transmembrane potential (ΔΨm), up-regulation of Bax and Bak, phosphatidylserine (PS) exposure, release of mitochondrial cytochrome c, and activation of caspase-8 and caspase-9 in human platelets. Furthermore, STS stimulation induced phosphorylation of p38 mitogen-activated protein kinase (MAPK). Inhibition of p38 MAPK activation significantly reduced ΔΨm depolarization and PS exposure in platelets stimulated with STS.
assistant
These data indicate that STS induces platelet apoptosis via the p38 MAPK signaling pathway. These findings suggest that platelet apoptosis-related hemorrhage should be noticed in STS and its derivatives in clinical tests. Final Decision: yes