Estrogen regulation of endothelial and smooth muscle cell migration and proliferation: Role of p38 and p42/44 mitogen-activated protein kinase
Restenosis is a major limitation of percutaneous coronary intervention. Migration and proliferation of vascular cells remain a cornerstone in neointimal formation. The cardioprotection of estrogen is well recognized, but the intracellular mechanisms related to these beneficial effects are not comple...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2002-10, Vol.22 (10), p.1585-1590 |
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| creator | GERALDES, Pedro SIROIS, Martin G BERNATCHEZ, Pascal N TANGUAY, Jean-Francois |
| description | Restenosis is a major limitation of percutaneous coronary intervention. Migration and proliferation of vascular cells remain a cornerstone in neointimal formation. The cardioprotection of estrogen is well recognized, but the intracellular mechanisms related to these beneficial effects are not completely understood.
We investigated the effects of 17beta-estradiol (17betaE) on mitogen-activated protein kinase (MAPK) activity and the migration and proliferation of porcine aortic endothelial cells (PAECs) and porcine smooth muscle cells (PSMCs). Treatment with 17betaE (10(-8) mol/L) abrogated p38 and p42/44 MAPK phosphorylation mediated by platelet-derived growth factor-BB as well as the migration and proliferation of PSMCs. In contrast, treatment with 17betaE (10(-8) mol/L) induced the phosphorylation of p38 and p42/44 MAPK and the migration and proliferation of PAECs. Interestingly, the effects of 17betaE on PSMCs and PAECs were reversed by selective estrogen receptor antagonists (tamoxifen, 4-OH-tamoxifen, and raloxifen). These results suggest that in PSMCs, 17betaE inhibits chemotactic and mitogenic effects of platelet-derived growth factor-BB as well as p38 and p42/44 MAPK phosphorylation. In contrast, 17betaE promotes in PAECs the phosphorylation of p42/44 and p38 MAPK as well as the migration and proliferation of these cells.
Treatment with 17betaE has a dual beneficial effect: the improvement of vascular healing and the prevention of restenosis after angioplasty. |
| doi_str_mv | 10.1161/01.ATV.0000035393.11854.6A |
| format | Article |
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We investigated the effects of 17beta-estradiol (17betaE) on mitogen-activated protein kinase (MAPK) activity and the migration and proliferation of porcine aortic endothelial cells (PAECs) and porcine smooth muscle cells (PSMCs). Treatment with 17betaE (10(-8) mol/L) abrogated p38 and p42/44 MAPK phosphorylation mediated by platelet-derived growth factor-BB as well as the migration and proliferation of PSMCs. In contrast, treatment with 17betaE (10(-8) mol/L) induced the phosphorylation of p38 and p42/44 MAPK and the migration and proliferation of PAECs. Interestingly, the effects of 17betaE on PSMCs and PAECs were reversed by selective estrogen receptor antagonists (tamoxifen, 4-OH-tamoxifen, and raloxifen). These results suggest that in PSMCs, 17betaE inhibits chemotactic and mitogenic effects of platelet-derived growth factor-BB as well as p38 and p42/44 MAPK phosphorylation. In contrast, 17betaE promotes in PAECs the phosphorylation of p42/44 and p38 MAPK as well as the migration and proliferation of these cells.
Treatment with 17betaE has a dual beneficial effect: the improvement of vascular healing and the prevention of restenosis after angioplasty.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000035393.11854.6A</identifier><identifier>PMID: 12377734</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: Lippincott</publisher><subject>Animals ; Aorta - cytology ; Aorta - drug effects ; Aorta - enzymology ; Aorta - metabolism ; Biological and medical sciences ; Cell Division - drug effects ; Cell Division - physiology ; Cell Movement - drug effects ; Cell Movement - physiology ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - enzymology ; Endothelium, Vascular - metabolism ; Estradiol - pharmacology ; Estrogens - physiology ; Hormones. Endocrine system ; MAP Kinase Signaling System - drug effects ; Medical sciences ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 1 - physiology ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases - metabolism ; Mitogen-Activated Protein Kinases - physiology ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - enzymology ; Muscle, Smooth, Vascular - metabolism ; p38 Mitogen-Activated Protein Kinases ; Pharmacology. Drug treatments ; Phosphorylation - drug effects ; Receptors, Estrogen - metabolism ; Swine ; Tunica Intima - drug effects ; Tunica Intima - enzymology ; Tunica Intima - metabolism</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2002-10, Vol.22 (10), p.1585-1590</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Oct 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-2e4ca42123f16033f1d88ad12abd2e9a843a7305f57911129bfb5ca84cbc6f653</citedby><cites>FETCH-LOGICAL-c407t-2e4ca42123f16033f1d88ad12abd2e9a843a7305f57911129bfb5ca84cbc6f653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13977981$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12377734$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GERALDES, Pedro</creatorcontrib><creatorcontrib>SIROIS, Martin G</creatorcontrib><creatorcontrib>BERNATCHEZ, Pascal N</creatorcontrib><creatorcontrib>TANGUAY, Jean-Francois</creatorcontrib><title>Estrogen regulation of endothelial and smooth muscle cell migration and proliferation: Role of p38 and p42/44 mitogen-activated protein kinase</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>Restenosis is a major limitation of percutaneous coronary intervention. Migration and proliferation of vascular cells remain a cornerstone in neointimal formation. The cardioprotection of estrogen is well recognized, but the intracellular mechanisms related to these beneficial effects are not completely understood.
We investigated the effects of 17beta-estradiol (17betaE) on mitogen-activated protein kinase (MAPK) activity and the migration and proliferation of porcine aortic endothelial cells (PAECs) and porcine smooth muscle cells (PSMCs). Treatment with 17betaE (10(-8) mol/L) abrogated p38 and p42/44 MAPK phosphorylation mediated by platelet-derived growth factor-BB as well as the migration and proliferation of PSMCs. In contrast, treatment with 17betaE (10(-8) mol/L) induced the phosphorylation of p38 and p42/44 MAPK and the migration and proliferation of PAECs. Interestingly, the effects of 17betaE on PSMCs and PAECs were reversed by selective estrogen receptor antagonists (tamoxifen, 4-OH-tamoxifen, and raloxifen). These results suggest that in PSMCs, 17betaE inhibits chemotactic and mitogenic effects of platelet-derived growth factor-BB as well as p38 and p42/44 MAPK phosphorylation. In contrast, 17betaE promotes in PAECs the phosphorylation of p42/44 and p38 MAPK as well as the migration and proliferation of these cells.
Treatment with 17betaE has a dual beneficial effect: the improvement of vascular healing and the prevention of restenosis after angioplasty.</description><subject>Animals</subject><subject>Aorta - cytology</subject><subject>Aorta - drug effects</subject><subject>Aorta - enzymology</subject><subject>Aorta - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - physiology</subject><subject>Cell Movement - drug effects</subject><subject>Cell Movement - physiology</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Estradiol - pharmacology</subject><subject>Estrogens - physiology</subject><subject>Hormones. Endocrine system</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 1 - physiology</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mitogen-Activated Protein Kinases - physiology</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - enzymology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation - drug effects</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Swine</subject><subject>Tunica Intima - drug effects</subject><subject>Tunica Intima - enzymology</subject><subject>Tunica Intima - metabolism</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkdtqHSEYhaW0NIf2FYoEmrvZ8TQ6k7tNSNJCoFCS3Irj6K6po7vqFPoSfeY6mQ0b6oWH32_9S1kAXGC0wZjjK4Q328fnDVoGbWlPa7lr2YZv34BT3BLWME7527pHom9azsgJOMv5peKMEPQenGBChRCUnYK_t7mkuDMBJrObvSouBhgtNGGM5YfxTnmowgjzFOsZTnPW3kBtvIeT26WVX4B9it5Zs1au4fdYsdpnT7v1mpErxqqmLGaN0sX9VsW86opxAf50QWXzAbyzymfz8bCeg6e728ebL83Dt_uvN9uHRjMkSkMM04qR-g2LOaJ1HrtOjZioYSSmVx2jSlDU2lb0GGPSD3ZodS3rQXPLW3oOLte-1f7XbHKRk8vLr1Qwcc5SEMw5ZayCF_-BL3FOob5NEsSqRc-7Cl2vkE4x52Ss3Cc3qfRHYiSXyCTCskYmj5HJ18gk31bxp4PDPExmPEoPGVXg8wFQWStvkwra5SNHeyH6DtN_lwmgJg</recordid><startdate>20021001</startdate><enddate>20021001</enddate><creator>GERALDES, Pedro</creator><creator>SIROIS, Martin G</creator><creator>BERNATCHEZ, Pascal N</creator><creator>TANGUAY, Jean-Francois</creator><general>Lippincott</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20021001</creationdate><title>Estrogen regulation of endothelial and smooth muscle cell migration and proliferation: Role of p38 and p42/44 mitogen-activated protein kinase</title><author>GERALDES, Pedro ; SIROIS, Martin G ; BERNATCHEZ, Pascal N ; TANGUAY, Jean-Francois</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c407t-2e4ca42123f16033f1d88ad12abd2e9a843a7305f57911129bfb5ca84cbc6f653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Aorta - cytology</topic><topic>Aorta - drug effects</topic><topic>Aorta - enzymology</topic><topic>Aorta - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Division - drug effects</topic><topic>Cell Division - physiology</topic><topic>Cell Movement - drug effects</topic><topic>Cell Movement - physiology</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Estradiol - pharmacology</topic><topic>Estrogens - physiology</topic><topic>Hormones. Endocrine system</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 1 - physiology</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Mitogen-Activated Protein Kinases - physiology</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - enzymology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation - drug effects</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Swine</topic><topic>Tunica Intima - drug effects</topic><topic>Tunica Intima - enzymology</topic><topic>Tunica Intima - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GERALDES, Pedro</creatorcontrib><creatorcontrib>SIROIS, Martin G</creatorcontrib><creatorcontrib>BERNATCHEZ, Pascal N</creatorcontrib><creatorcontrib>TANGUAY, Jean-Francois</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GERALDES, Pedro</au><au>SIROIS, Martin G</au><au>BERNATCHEZ, Pascal N</au><au>TANGUAY, Jean-Francois</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen regulation of endothelial and smooth muscle cell migration and proliferation: Role of p38 and p42/44 mitogen-activated protein kinase</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2002-10-01</date><risdate>2002</risdate><volume>22</volume><issue>10</issue><spage>1585</spage><epage>1590</epage><pages>1585-1590</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>Restenosis is a major limitation of percutaneous coronary intervention. Migration and proliferation of vascular cells remain a cornerstone in neointimal formation. The cardioprotection of estrogen is well recognized, but the intracellular mechanisms related to these beneficial effects are not completely understood.
We investigated the effects of 17beta-estradiol (17betaE) on mitogen-activated protein kinase (MAPK) activity and the migration and proliferation of porcine aortic endothelial cells (PAECs) and porcine smooth muscle cells (PSMCs). Treatment with 17betaE (10(-8) mol/L) abrogated p38 and p42/44 MAPK phosphorylation mediated by platelet-derived growth factor-BB as well as the migration and proliferation of PSMCs. In contrast, treatment with 17betaE (10(-8) mol/L) induced the phosphorylation of p38 and p42/44 MAPK and the migration and proliferation of PAECs. Interestingly, the effects of 17betaE on PSMCs and PAECs were reversed by selective estrogen receptor antagonists (tamoxifen, 4-OH-tamoxifen, and raloxifen). These results suggest that in PSMCs, 17betaE inhibits chemotactic and mitogenic effects of platelet-derived growth factor-BB as well as p38 and p42/44 MAPK phosphorylation. In contrast, 17betaE promotes in PAECs the phosphorylation of p42/44 and p38 MAPK as well as the migration and proliferation of these cells.
Treatment with 17betaE has a dual beneficial effect: the improvement of vascular healing and the prevention of restenosis after angioplasty.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>12377734</pmid><doi>10.1161/01.ATV.0000035393.11854.6A</doi><tpages>6</tpages></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2002-10, Vol.22 (10), p.1585-1590 |
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| source | Journals@Ovid Ovid Autoload; MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Aorta - cytology Aorta - drug effects Aorta - enzymology Aorta - metabolism Biological and medical sciences Cell Division - drug effects Cell Division - physiology Cell Movement - drug effects Cell Movement - physiology Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - enzymology Endothelium, Vascular - metabolism Estradiol - pharmacology Estrogens - physiology Hormones. Endocrine system MAP Kinase Signaling System - drug effects Medical sciences Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 1 - physiology Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases - metabolism Mitogen-Activated Protein Kinases - physiology Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - enzymology Muscle, Smooth, Vascular - metabolism p38 Mitogen-Activated Protein Kinases Pharmacology. Drug treatments Phosphorylation - drug effects Receptors, Estrogen - metabolism Swine Tunica Intima - drug effects Tunica Intima - enzymology Tunica Intima - metabolism |
| title | Estrogen regulation of endothelial and smooth muscle cell migration and proliferation: Role of p38 and p42/44 mitogen-activated protein kinase |
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