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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
1993-9-30
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pubmed:abstractText |
The significance and mechanism of extracellular calcium influx in the stimulation by PDGF of cell replication was investigated in density-arrested C3H 10T1/2 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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/8-(N,N-diethylamino)octyl-3,4,5-trim...,
http://linkedlifedata.com/resource/pubmed/chemical/Bucladesine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Gallic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Lanthanum,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet-Derived Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0143-4160
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
439-54
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:8395338-Animals,
pubmed-meshheading:8395338-Bucladesine,
pubmed-meshheading:8395338-Calcium,
pubmed-meshheading:8395338-Calcium Channels,
pubmed-meshheading:8395338-Cell Compartmentation,
pubmed-meshheading:8395338-Cell Division,
pubmed-meshheading:8395338-Cell Line,
pubmed-meshheading:8395338-Cell Membrane,
pubmed-meshheading:8395338-Contact Inhibition,
pubmed-meshheading:8395338-DNA Replication,
pubmed-meshheading:8395338-Drug Synergism,
pubmed-meshheading:8395338-Extracellular Space,
pubmed-meshheading:8395338-Fibroblasts,
pubmed-meshheading:8395338-Forskolin,
pubmed-meshheading:8395338-Gallic Acid,
pubmed-meshheading:8395338-Insulin,
pubmed-meshheading:8395338-Ion Channel Gating,
pubmed-meshheading:8395338-Lanthanum,
pubmed-meshheading:8395338-Mice,
pubmed-meshheading:8395338-Mice, Inbred C3H,
pubmed-meshheading:8395338-Nifedipine,
pubmed-meshheading:8395338-Platelet-Derived Growth Factor,
pubmed-meshheading:8395338-S Phase,
pubmed-meshheading:8395338-Signal Transduction,
pubmed-meshheading:8395338-Tetradecanoylphorbol Acetate
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pubmed:year |
1993
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pubmed:articleTitle |
Competence induction by PDGF requires sustained calcium influx by a mechanism distinct from storage-dependent calcium influx.
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pubmed:affiliation |
University of Hawaii at Manoa, Cancer Research Center of Hawaii, Honolulu.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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