Lysosome inhibitors enhance the ability of cyclic AMP-elevating agents to induce the LDL receptor in human vascular smooth muscle cells
Identifieur interne : 002E69 ( Main/Exploration ); précédent : 002E68; suivant : 002E70Lysosome inhibitors enhance the ability of cyclic AMP-elevating agents to induce the LDL receptor in human vascular smooth muscle cells
Auteurs : Bruce Middleton [Royaume-Uni]Source :
- Biochemical and Biophysical Research Communications [ 0006-291X ] ; 1992.
English descriptors
- KwdEn :
- Teeft :
- Additively, Biophys, Biophysical research communications, Cell surface, Cellular cholesterol, Cellular cyclic, Chloroquine, Cholesterol synthesis, Cholesteryl, Cholesteryl ester, Confusing diversity, Cultured cells, Cyclic, Dmem, Dmso, Ester, Forskolin, Forskolin stimulation, Goldstein, Hvsmc, Inhibitor, Lpdm, Lysosomal, Lysosomal function, Lysosome, Metabolism, Methionine, Mevinolin, Middleton, Muscle cells, Pathway, Preincubation, Prostaglandin, Protein synthesis, Receptor, Receptor activity, Receptor expression, Receptor number, Receptor pathway, Receptor protein, Receptor synthesis, Reductase, Serum albumin, Smooth muscle cells.
Abstract
Abstract: In human vascular smooth muscle cells cyclic AMP elevation by forskolin increases synthesis of the LDL receptor by a mechanism which appears independent of sterol control. This increased receptor synthesis is further enhanced by chloroquine. Both forskolin and prostaglandin E1 increase the number of cell surface LDL receptors indicating that prostaglandins could exert physiological control over LDL metabolism. This effect is enhanced synergistically by chloroquine. The stimulation by forskolin of LDL receptor synthesis and expression leads to increased metabolism of apo-B and increased hydrolysis of LDL-borne cholesteryl ester. These effects of cyclic AMP on the activity of the LDL pathway are enhanced more than additively by preincubation with the reversible lysosomal inhibitor NH4Cl. Thus cyclic AMP causes upregulation of the LDL receptor pathway resulting in increased rates of LDL metabolism but this effect can be damped or masked in cell culture by a cyclic AMP-sensitive lysosomal event, probably the acute stimulation of lysosomal cholesterol ester hydrolase.
Url:
DOI: 10.1016/0006-291X(92)91807-3
Affiliations:
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Lysosome inhibitors enhance the ability of cyclic AMP-elevating agents to induce the LDL receptor in human vascular smooth muscle cells</title><author><name sortKey="Middleton, Bruce" sort="Middleton, Bruce" uniqKey="Middleton B" first="Bruce" last="Middleton">Bruce Middleton</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:CCD54F89444CCA9798F8B901F54605089C244A50</idno><date when="1992" year="1992">1992</date><idno type="doi">10.1016/0006-291X(92)91807-3</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-HL48BRBD-N/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000A11</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000A11</idno><idno type="wicri:Area/Istex/Curation">000A11</idno><idno type="wicri:Area/Istex/Checkpoint">001C42</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001C42</idno><idno type="wicri:doubleKey">0006-291X:1992:Middleton B:lysosome:inhibitors:enhance</idno><idno type="wicri:Area/Main/Merge">002F35</idno><idno type="wicri:Area/Main/Curation">002E69</idno><idno type="wicri:Area/Main/Exploration">002E69</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Lysosome inhibitors enhance the ability of cyclic AMP-elevating agents to induce the LDL receptor in human vascular smooth muscle cells</title><author><name sortKey="Middleton, Bruce" sort="Middleton, Bruce" uniqKey="Middleton B" first="Bruce" last="Middleton">Bruce Middleton</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Biochemistry, University of Nottingham Medical School, Queen's Medical Centre, Nottingham NG7 2UH, England</wicri:regionArea><wicri:noRegion>England</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Biochemical and Biophysical Research Communications</title><title level="j" type="abbrev">YBBRC</title><idno type="ISSN">0006-291X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1992">1992</date><biblScope unit="volume">182</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="830">830</biblScope><biblScope unit="page" to="835">835</biblScope></imprint><idno type="ISSN">0006-291X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-291X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DMEM</term><term>DMSO</term><term>DPBS</term><term>HMG-CoA</term><term>HVSMC</term><term>LDL</term><term>LPDM</term><term>SDS PAGE</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Additively</term><term>Biophys</term><term>Biophysical research communications</term><term>Cell surface</term><term>Cellular cholesterol</term><term>Cellular cyclic</term><term>Chloroquine</term><term>Cholesterol synthesis</term><term>Cholesteryl</term><term>Cholesteryl ester</term><term>Confusing diversity</term><term>Cultured cells</term><term>Cyclic</term><term>Dmem</term><term>Dmso</term><term>Ester</term><term>Forskolin</term><term>Forskolin stimulation</term><term>Goldstein</term><term>Hvsmc</term><term>Inhibitor</term><term>Lpdm</term><term>Lysosomal</term><term>Lysosomal function</term><term>Lysosome</term><term>Metabolism</term><term>Methionine</term><term>Mevinolin</term><term>Middleton</term><term>Muscle cells</term><term>Pathway</term><term>Preincubation</term><term>Prostaglandin</term><term>Protein synthesis</term><term>Receptor</term><term>Receptor activity</term><term>Receptor expression</term><term>Receptor number</term><term>Receptor pathway</term><term>Receptor protein</term><term>Receptor synthesis</term><term>Reductase</term><term>Serum albumin</term><term>Smooth muscle cells</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: In human vascular smooth muscle cells cyclic AMP elevation by forskolin increases synthesis of the LDL receptor by a mechanism which appears independent of sterol control. This increased receptor synthesis is further enhanced by chloroquine. Both forskolin and prostaglandin E1 increase the number of cell surface LDL receptors indicating that prostaglandins could exert physiological control over LDL metabolism. This effect is enhanced synergistically by chloroquine. The stimulation by forskolin of LDL receptor synthesis and expression leads to increased metabolism of apo-B and increased hydrolysis of LDL-borne cholesteryl ester. These effects of cyclic AMP on the activity of the LDL pathway are enhanced more than additively by preincubation with the reversible lysosomal inhibitor NH4Cl. Thus cyclic AMP causes upregulation of the LDL receptor pathway resulting in increased rates of LDL metabolism but this effect can be damped or masked in cell culture by a cyclic AMP-sensitive lysosomal event, probably the acute stimulation of lysosomal cholesterol ester hydrolase.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Middleton, Bruce" sort="Middleton, Bruce" uniqKey="Middleton B" first="Bruce" last="Middleton">Bruce Middleton</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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