Linked Life Data

20428447

Source:http://linkedlifedata.com/resource/pubmed/id/20428447

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pubmed-article:20428447pubmed:dateCreated2010-4-29lld:pubmed
pubmed-article:20428447pubmed:abstractTextNumerous steroids are now believed to possess rapid membrane effects independent of the classical gene activation pathways and are potent modulators of membrane proteins, including voltage-and ligand-operated channels. The effects of steroids on the functional state of the intercellular channels clustered in gap junctions were compared by estimation of either the permeability for a fluorescent dye or the electrical conductance in cardiac myocytes of newborn rat. At 25 muM, the esters of 17beta-estradiol, testosterone and two other androgen hormones rapidly abolished cell-to-cell communication, whereas none of the longer chain steroids, belonging to pregnane (17alpha-hydroxypregnenolone, hydrocortisone), sterol (cholesterol, 25-hydroxycholesterol), bile acid (cholic and lithocholic acids) and vitamin (D3) families, lowered the junctional permeability. Altogether, no correlation with the presence or position of double bonds nor with the trans- or cis-fusion of the A and B rings was recognized. Esterification was a prerequisite for the activity of extracellularly applied steroids but the number, nature and position of ester chain(s) had no influence. 17beta-estradiol or testosterone effects were not prevented when cells were prein-cubated with blockers of the estrogen or androgen nuclear receptors (tamoxifen and cyproterone acetate, respectively). This, together with the rapid time course of the steroid effect (complete within a few minutes), in a rather high active concentration range, suggests a nongenomic mechanism of action. The reversible uncoupling effect of steroids appears to be independent of the shape of the molecules and more probably related to their size and lipo-solubility, which condition their insertion into the lipid bilayer and their subsequent disturbing effects.lld:pubmed
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pubmed-article:20428447pubmed:statusPubMed-not-MEDLINElld:pubmed
pubmed-article:20428447pubmed:issn1918-1515lld:pubmed
pubmed-article:20428447pubmed:authorpubmed-author:SarrouilheDDlld:pubmed
pubmed-article:20428447pubmed:authorpubmed-author:HervéJ CJClld:pubmed
pubmed-article:20428447pubmed:authorpubmed-author:VerrecchiaFFlld:pubmed
pubmed-article:20428447pubmed:issnTypeElectroniclld:pubmed
pubmed-article:20428447pubmed:volume6lld:pubmed
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pubmed-article:20428447pubmed:pagination124-31lld:pubmed
pubmed-article:20428447pubmed:year2001lld:pubmed
pubmed-article:20428447pubmed:articleTitleNongenomic steroid action: Inhibiting effects on cell-to-cell communication between rat ventricular myocytes.lld:pubmed
pubmed-article:20428447pubmed:affiliationPhysiologie Cellulaire, UMR CNRS 6558.lld:pubmed
pubmed-article:20428447pubmed:publicationTypeJournal Articlelld:pubmed