Inhibition of early platelet-derived growth factor responses in BALB c-3T3 cells by interferon

M. Zagari; J. R. Hepler; C. Harris; B. Herman

doi:10.1016/0006-291X(88)90757-7

Inhibition of early platelet-derived growth factor responses in BALB c-3T3 cells by interferon

M. Zagari, J. R. Hepler, C. Harris, B. Herman

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

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 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)
Pages (from-to)	1207-1212
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	150
Issue number	3
DOIs	https://doi.org/10.1016/0006-291X(88)90757-7
State	Published - Feb 15 1988
Externally published	Yes

Bibliographical note

Funding 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.

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title = "Inhibition of early platelet-derived growth factor responses in BALB c-3T3 cells by interferon",

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 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.",

author = "M. Zagari and Hepler, {J. R.} and C. Harris and B. Herman",

note = "Funding 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.",

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AU - Zagari, M.

AU - Hepler, J. R.

AU - Harris, C.

AU - Herman, B.

N1 - Funding 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.

PY - 1988/2/15

Y1 - 1988/2/15

N2 - 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.

AB - 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.

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Inhibition of early platelet-derived growth factor responses in BALB c-3T3 cells by interferon

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