Abstract
Stimulation of total inositol phosphate production, alteration of cytosolic free calcium ([Ca++]i), vinculin disruption from adhesion plaques, and DNA synthesis caused by PDGF were examined in normal and INF pretreated density arrested BALBc-3T3 fibroblasts. In normal cells, PDGF caused an increase in total inositol phosphates, a rapid, transient increase in [Ca++]i, disappearance of vinculin from adhesion plaques, and stimulation of DNA synthesis. Pretreatment of cells with INF inhibited PDGF-stimulated increases in [Ca++]i, vinculin disruption from adhesion plaques, and DNA synthesis, but had no effect of PDGF-induced increase in total inositol phosphate levels. These findings suggest that INF prevents entry of quiescent BALBc-3T3 cells into G1 by inhibiting PDGF-induced release of Ca++ from intracellular stores.
Published Version
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