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 BALB c-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 BALB c-3T3 cells into G1 by inhibiting PDGF-induced release of Ca++ from intracellular stores.
|Original language||English (US)|
|Number of pages||6|
|Journal||Biochemical and Biophysical Research Communications|
|State||Published - Feb 15 1988|
Bibliographical noteFunding Information:
ACKNOWLEDGEMENTTSh: is work was supported by grants from the American Heart Association (AHA 861299, NC-AHA 86-87-02) and from NIH (AG07218). We thank Marcy Stephens for performing the [3H]-thymidine assays.