Programmed Anuclear Cell Death Delimits Platelet Life Span

摘要: Platelets are anuclear cytoplasmic fragments essential for blood clotting and wound healing. Despite much speculation, the factors determining their life span in circulation unknown. We show here that an intrinsic program apoptosis controls platelet survival dictates span. Pro-survival Bcl-x L constrains pro-apoptotic activity of Bak to maintain survival, but as degrades, aged platelets primed cell death. Genetic ablation or pharmacological inactivation reduces half-life causes thrombocytopenia a dose-dependent manner. Deletion corrects these defects, from Bak-deficient mice live longer than normal. Thus, are, by default, genetically programmed die apoptosis. The antagonistic balance between constitutes molecular clock determines span: this represents important paradigm cellular homeostasis, has profound implications diagnosis treatment disorders affect number function.