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• W2056588209 abstract "The significance and mechanism of extracellular calcium influx in the stimulation by PDGF of cell replication was investigated in density-arrested C3H 10T12 mouse fibroblasts. PDGF consistently stimulated a biphasic increase in the [Ca2+]i composed of a rapid transient release of calcium from intracellular storage sites followed by a sustained elevation, significantly greater than prestimulated levels, which was dependent upon the [Ca2+]e and persisted for at least 1 h. The percentage of cells incorporating [3H]-TdR into DNA after stimulation with PDGF + insulin was closely correlated with the magnitude of the sustained [Ca2+]i increase and to the [Ca2+]e. Selective inhibition of the sustained [Ca2+]i increase, by blocking calcium influx with La3+, completely inhibited progression to S phase without affecting the release of calcium from intracellular storage sites. Progression to S phase was inhibited by La3+ or the omission of added extracellular calcium only during PDGF exposure and not during treatment with insulin. PDGF-induced calcium influx was completely inhibited by La3+ whereas storage-dependent calcium influx (SDCI) induced by thapsigargin was unaffected. Pretreatment with TPA, forskolin, dibutyryl-cAMP, dibutyryl-cGMP, nifedipine, and TMB-8 had no effect on PDGF-induced calcium influx. These data suggest that the induction of replicative competence by PDGF is dependent upon the maintenance of a sustained increase in the intracellular calcium concentration due to the influx of extracellular calcium through a calcium influx pathway distinct from SDCI." @default.
• W2056588209 created "2016-06-24" @default.
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• W2056588209 creator A5055810968 @default.
• W2056588209 date "1993-06-01" @default.
• W2056588209 modified "2023-10-17" @default.
• W2056588209 title "Competence induction by PDGF requires sustained calcium influx by a mechanism distinct from storage-dependent calcium influx" @default.
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• W2056588209 doi "https://doi.org/10.1016/0143-4160(93)90003-o" @default.
• W2056588209 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8395338" @default.
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