Dexamethasone affects phosphatidylinositol synthesis and degradation in cultured human embryonic cells
Dexamethasone (DEX), a glucocorticoid which induces cleft palate, causes marked alterations in the synthesis and degradation of phosphatidylinositol (PI) but not phosphatidylcholine in an established fibroblastic cell line derived from a human embryonic palate. Incorporation of radiolabeled inositol...
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Veröffentlicht in: | Biochemical and biophysical research communications 1983-01, Vol.110 (1), p.200-207 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Dexamethasone (DEX), a glucocorticoid which induces cleft palate, causes marked alterations in the synthesis and degradation of phosphatidylinositol (PI) but not phosphatidylcholine in an established fibroblastic cell line derived from a human embryonic palate. Incorporation of radiolabeled inositol into phosphatidylinositol as well as degradation of prelabeled phosphatidylinositol is stimulated by DEX. The dose-response curves for the DEX-induced effect on PI synthesis and DEX-induced inhibition of cell proliferation are nearly identical, with the maximal responses occurring at 10
−8M DEX. Our results suggest that DEX-induced inhibition of human embryonic palatal mesenchyme cell proliferation and alterations in synthesis and degradation of phosphatidylinositol are related. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/0006-291X(83)91280-9 |