Overexpression of Protein Kinase C Isoform ’ but not δ in Human Interleukin-3–Dependent Cells Suppresses Apoptosis and Induces bcl-2 Expression

摘要: Hematopoietic progenitor cells die by apoptosis after removal of the appropriate colony-stimulating factor (CSF). Recent pharmacologic data have implicated protein kinase C (PKC) in suppression interleukin-3 (IL-3) and granulocyte-macrophage (GM)-CSF–dependent human myeloid cells. Because IL-3 GM-CSF induce increases diacylglycerol without mobilizing intracellular Ca++, it seemed that one novel Ca++ independent isoforms PKC was involved. We report here overexpression PKC factor-dependent TF-1 extends cell survival absence cytokine. Overexpression PKCδ does not this effect. By 72 to 96 hours cytokine withdrawal, transfectants remain distributed all phases cycle, as shown fluorescence-activated sorting (FACS) analysis, while little intact cellular DNA is detectable vector or transfectants. induces bcl-2 expression fivefold sixfold over levels empty transfectants, whereas are similar those controls.