Regulatory mechanisms for thrombomodulin expression in human umbilical vein endothelial cells in vitro
Identifieur interne : 002F61 ( Main/Exploration ); précédent : 002F60; suivant : 002F62Regulatory mechanisms for thrombomodulin expression in human umbilical vein endothelial cells in vitro
Auteurs : Kazunori Hirokawa [Japon] ; Nobuo Aoki [Japon]Source :
- Journal of Cellular Physiology [ 0021-9541 ] ; 1991-04.
Abstract
It has been reported that thrombomodulin (TM) expression in endothelial cells is modulated by various agents. We investigated cellular regulatory mechanisms for TM expression in human umbilical vein endothelial cells (HUVECs), incubated with agents, by measuring the time course changes in surface TM activity, total TM antigen in cell lysates, and TM mRNA levels. While dibutyryl cAMP (3 mM) increased TM mRNA levels in HUVECs and was followed by increased TM activity, dibutyryl cGMP had no effect on TM activity. Phorbol myristate acetate (PMA) induced rapid loss of surface TM activity (∼8 h) and later increased TM mRNA levels between 4 h and 40 h (maximum at 24 h), resulting in biphasic effects on TM activity. Tumor necrosis factor or interleukin‐1β suppressed surface TM activity and TM mRNA levels. Internalization/degradation of TM in HUVECs incubated with PMA or cytokines was suggested by co‐culture with chloroquine. The decrease in surface TM activity observed was not caused by the release of TM molecules from the cells into the conditioned media. These results suggest that TM activity in HUVECs is modulated by independent mechanisms involving cytoplasmic TM mRNA levels and internalization/degradation of TM molecules. These regulatory mechanisms may involve protein kinase A and protein kinase C‐dependent mechanisms but are independent of protein kinase G.
Url:
DOI: 10.1002/jcp.1041470120
Affiliations:
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Regulatory mechanisms for thrombomodulin expression in human umbilical vein endothelial cells in vitro</title><author><name sortKey="Hirokawa, Kazunori" sort="Hirokawa, Kazunori" uniqKey="Hirokawa K" first="Kazunori" last="Hirokawa">Kazunori Hirokawa</name></author><author><name sortKey="Aoki, Nobuo" sort="Aoki, Nobuo" uniqKey="Aoki N" first="Nobuo" last="Aoki">Nobuo Aoki</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8628A52CD1C774FA3B4DA6F7141A262EAAABB721</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1002/jcp.1041470120</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-6QZNHFGZ-B/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000905</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000905</idno><idno type="wicri:Area/Istex/Curation">000905</idno><idno type="wicri:Area/Istex/Checkpoint">001D32</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001D32</idno><idno type="wicri:doubleKey">0021-9541:1991:Hirokawa K:regulatory:mechanisms:for</idno><idno type="wicri:Area/Main/Merge">003028</idno><idno type="wicri:Area/Main/Curation">002F61</idno><idno type="wicri:Area/Main/Exploration">002F61</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Regulatory mechanisms for thrombomodulin expression in human umbilical vein endothelial cells in vitro</title><author><name sortKey="Hirokawa, Kazunori" sort="Hirokawa, Kazunori" uniqKey="Hirokawa K" first="Kazunori" last="Hirokawa">Kazunori Hirokawa</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Tokyo Medical and Dental University, Yushima, Bunkyo‐ku, Tokyo 113</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Aoki, Nobuo" sort="Aoki, Nobuo" uniqKey="Aoki N" first="Nobuo" last="Aoki">Nobuo Aoki</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Tokyo Medical and Dental University, Yushima, Bunkyo‐ku, Tokyo 113</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Correspondence address: First Department of Medicine, Tokyo Medical and Dental University, Yushima, Bunkyo‐ku, Tokyo 113</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Cellular Physiology</title><title level="j" type="alt">JOURNAL OF CELLULAR PHYSIOLOGY</title><idno type="ISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><imprint><biblScope unit="vol">147</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="157">157</biblScope><biblScope unit="page" to="165">165</biblScope><biblScope unit="page-count">9</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1991-04">1991-04</date></imprint><idno type="ISSN">0021-9541</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It has been reported that thrombomodulin (TM) expression in endothelial cells is modulated by various agents. We investigated cellular regulatory mechanisms for TM expression in human umbilical vein endothelial cells (HUVECs), incubated with agents, by measuring the time course changes in surface TM activity, total TM antigen in cell lysates, and TM mRNA levels. While dibutyryl cAMP (3 mM) increased TM mRNA levels in HUVECs and was followed by increased TM activity, dibutyryl cGMP had no effect on TM activity. Phorbol myristate acetate (PMA) induced rapid loss of surface TM activity (∼8 h) and later increased TM mRNA levels between 4 h and 40 h (maximum at 24 h), resulting in biphasic effects on TM activity. Tumor necrosis factor or interleukin‐1β suppressed surface TM activity and TM mRNA levels. Internalization/degradation of TM in HUVECs incubated with PMA or cytokines was suggested by co‐culture with chloroquine. The decrease in surface TM activity observed was not caused by the release of TM molecules from the cells into the conditioned media. These results suggest that TM activity in HUVECs is modulated by independent mechanisms involving cytoplasmic TM mRNA levels and internalization/degradation of TM molecules. These regulatory mechanisms may involve protein kinase A and protein kinase C‐dependent mechanisms but are independent of protein kinase G.</div></front></TEI><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement></list><tree><country name="Japon"><region name="Région de Kantō"><name sortKey="Hirokawa, Kazunori" sort="Hirokawa, Kazunori" uniqKey="Hirokawa K" first="Kazunori" last="Hirokawa">Kazunori Hirokawa</name></region><name sortKey="Aoki, Nobuo" sort="Aoki, Nobuo" uniqKey="Aoki N" first="Nobuo" last="Aoki">Nobuo Aoki</name><name sortKey="Aoki, Nobuo" sort="Aoki, Nobuo" uniqKey="Aoki N" first="Nobuo" last="Aoki">Nobuo Aoki</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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