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rdf:type |
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lifeskim:mentions |
umls-concept:C0007961,
umls-concept:C0017262,
umls-concept:C0026649,
umls-concept:C0202220,
umls-concept:C0439799,
umls-concept:C0596235,
umls-concept:C1546426,
umls-concept:C1548280,
umls-concept:C1706211,
umls-concept:C1882854,
umls-concept:C2349975
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pubmed:dateCreated |
1999-6-29
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pubmed:abstractText |
1. We investigated whether insulin-like growth factor-1 (IGF-1), an endogenous potent activator of skeletal muscle proliferation and differentiation, enhances L-type Ca2+ channel gene expression resulting in increased functional voltage sensors in single skeletal muscle cells. 2. Charge movement and inward Ca2+ current were recorded in primary cultured rat myoballs using the whole-cell configuration of the patch-clamp technique. Ca2+ current and maximum charge movement (Qmax) were potentiated in cells treated with IGF-1 without significant changes in their voltage dependence. Peak Ca2+ current in control and IGF-1-treated cells was -7.8 +/- 0.44 and -10. 5 +/- 0.37 pA pF-1, respectively (P < 0.01), whilst Qmax was 12.9 +/- 0.4 and 22.0 +/- 0.3 nC microF-1, respectively (P < 0.01). 3. The number of L-type Ca2+ channels was found to increase in the same preparation. The maximum binding capacity (Bmax) of the high-affinity radioligand [3H]PN200-110 in control and IGF-1-treated cells was 1.21 +/- 0.25 and 3.15 +/- 0.5 pmol (mg protein)-1, respectively (P < 0.01). No significant change in the dissociation constant for [3H]PN200-110 was found. 4. Antisense RNA amplification showed a significant increase in the level of mRNA encoding the L-type Ca2+ channel alpha1-subunit in IGF-1-treated cells. 5. This study demonstrates that IGF-1 regulates charge movement and the level of L-type Ca2+ channel alpha1-subunits through activation of gene expression in skeletal muscle cells.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-1328616,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-1387410,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-1557406,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-1718988,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-1903391,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-2165571,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-2212982,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-2348406,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-2419568,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-2458430,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-2650560,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-3037387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-3142689,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-3795082,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-4540479,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-7540132,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-7699362,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-7742348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-7744859,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8010748,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8022415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8063821,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8119189,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8141261,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8169595,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8583414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8747553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8793181,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-8897022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-9178612,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-9207239,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-9247137,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-9278527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-9292730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10087334-9395065
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
516 ( Pt 2)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
331-41
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10087334-Animals,
pubmed-meshheading:10087334-Calcium Channels,
pubmed-meshheading:10087334-Calcium Channels, L-Type,
pubmed-meshheading:10087334-Electric Stimulation,
pubmed-meshheading:10087334-Electrophysiology,
pubmed-meshheading:10087334-Gene Expression Regulation,
pubmed-meshheading:10087334-Insulin-Like Growth Factor I,
pubmed-meshheading:10087334-Isradipine,
pubmed-meshheading:10087334-Membrane Potentials,
pubmed-meshheading:10087334-Muscle, Skeletal,
pubmed-meshheading:10087334-Patch-Clamp Techniques,
pubmed-meshheading:10087334-RNA, Antisense,
pubmed-meshheading:10087334-RNA, Messenger,
pubmed-meshheading:10087334-Rats,
pubmed-meshheading:10087334-Rats, Sprague-Dawley
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pubmed:year |
1999
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pubmed:articleTitle |
Insulin-like growth factor-1 enhances rat skeletal muscle charge movement and L-type Ca2+ channel gene expression.
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pubmed:affiliation |
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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