Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells
Mineralocorticoid receptor blockade protects from angiotensin II–induced target-organ damage. 11β-Hydroxysteroid dehydrogenase type 2 protects the mineralocorticoid receptor from activation by glucocorticoids; however, high glucocorticoid concentrations and absent 11β-hydroxysteroid dehydrogenase ty...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2008-05, Vol.51 (5), p.1372-1378 |
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| creator | Molnar, Gergö A Lindschau, Carsten Dubrovska, Galyna Mertens, Peter R Kirsch, Torsten Quinkler, Marcus Gollasch, Maik Wresche, Stefanie Luft, Friedrich C Muller, Dominik N Fiebeler, Anette |
| description | Mineralocorticoid receptor blockade protects from angiotensin II–induced target-organ damage. 11β-Hydroxysteroid dehydrogenase type 2 protects the mineralocorticoid receptor from activation by glucocorticoids; however, high glucocorticoid concentrations and absent 11β-hydroxysteroid dehydrogenase type 2 in some tissues make glucocorticoids highly relevant mineralocorticoid receptor ligands. We investigated the effects of corticosterone (10 to 10 mol/L) on early vascular mineralocorticoid receptor signaling by Western blotting, confocal microscopy, and myography. Corticosterone initiated extracellular signal–regulated kinase 1/2 phosphorylation in rat vascular smooth muscle cells at ≥10 mol/L doses. Protein synthesis inhibitors had no effect, indicating a nongenomic action. Corticosterone also stimulated c-Jun N-terminal kinase, p38, Src, and Akt phosphorylation at 15 minutes and enhanced angiotensin II–induced signaling at 5 minutes. A specific epidermal growth factor receptor blocker, AG1478, as well as the Src inhibitor PP2, markedly reduced corticosterone-induced extracellular signal–regulated kinase 1/2 phosphorylation, as did preincubation of cells with the mineralocorticoid receptor antagonist spironolactone. Silencing mineralocorticoid receptor with small interfering RNA abolished corticosterone-induced effects. Corticosterone (10 mol/L) enhanced phenylephrine-induced contraction of intact aortic rings. These effects were dependent on the intact endothelium, mineralocorticoid receptor, and mitogen-activated protein kinase kinase 1/extracellular signal-regulated kinase signaling. We conclude that corticosterone induces rapid mineralocorticoid receptor signaling in vascular smooth muscle cells that involves mitogen-activated protein kinase kinase/extracellular signal–regulated kinase–dependent pathways. These new mineralocorticoid receptor–dependent signaling pathways suggest that glucocorticoids may contribute to vascular disease via mineralocorticoid receptor signaling, independent of circulating aldosterone. |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.107.105718 |
| format | Article |
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We investigated the effects of corticosterone (10 to 10 mol/L) on early vascular mineralocorticoid receptor signaling by Western blotting, confocal microscopy, and myography. Corticosterone initiated extracellular signal–regulated kinase 1/2 phosphorylation in rat vascular smooth muscle cells at ≥10 mol/L doses. Protein synthesis inhibitors had no effect, indicating a nongenomic action. Corticosterone also stimulated c-Jun N-terminal kinase, p38, Src, and Akt phosphorylation at 15 minutes and enhanced angiotensin II–induced signaling at 5 minutes. A specific epidermal growth factor receptor blocker, AG1478, as well as the Src inhibitor PP2, markedly reduced corticosterone-induced extracellular signal–regulated kinase 1/2 phosphorylation, as did preincubation of cells with the mineralocorticoid receptor antagonist spironolactone. Silencing mineralocorticoid receptor with small interfering RNA abolished corticosterone-induced effects. Corticosterone (10 mol/L) enhanced phenylephrine-induced contraction of intact aortic rings. These effects were dependent on the intact endothelium, mineralocorticoid receptor, and mitogen-activated protein kinase kinase 1/extracellular signal-regulated kinase signaling. We conclude that corticosterone induces rapid mineralocorticoid receptor signaling in vascular smooth muscle cells that involves mitogen-activated protein kinase kinase/extracellular signal–regulated kinase–dependent pathways. These new mineralocorticoid receptor–dependent signaling pathways suggest that glucocorticoids may contribute to vascular disease via mineralocorticoid receptor signaling, independent of circulating aldosterone.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.107.105718</identifier><identifier>PMID: 18347231</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism ; Animals ; Aorta - drug effects ; Aorta - metabolism ; Aorta - pathology ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Cardiology. Vascular system ; Cells, Cultured ; Corticosterone - pharmacology ; Dose-Response Relationship, Drug ; Fundamental and applied biological sciences. Psychology ; JNK Mitogen-Activated Protein Kinases - metabolism ; MAP Kinase Kinase 1 - metabolism ; Medical sciences ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation - drug effects ; Protein-Tyrosine Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Mineralocorticoid - drug effects ; Receptors, Mineralocorticoid - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; src-Family Kinases ; Vasoconstriction - drug effects ; Vertebrates: cardiovascular system</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2008-05, Vol.51 (5), p.1372-1378</ispartof><rights>2008 American Heart Association, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4862-5c4d25dbdb2188c674a0eb5fbf35cf4691740fb64455b832115359aec612a8953</citedby><cites>FETCH-LOGICAL-c4862-5c4d25dbdb2188c674a0eb5fbf35cf4691740fb64455b832115359aec612a8953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3678,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20290312$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18347231$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Molnar, Gergö A</creatorcontrib><creatorcontrib>Lindschau, Carsten</creatorcontrib><creatorcontrib>Dubrovska, Galyna</creatorcontrib><creatorcontrib>Mertens, Peter R</creatorcontrib><creatorcontrib>Kirsch, Torsten</creatorcontrib><creatorcontrib>Quinkler, Marcus</creatorcontrib><creatorcontrib>Gollasch, Maik</creatorcontrib><creatorcontrib>Wresche, Stefanie</creatorcontrib><creatorcontrib>Luft, Friedrich C</creatorcontrib><creatorcontrib>Muller, Dominik N</creatorcontrib><creatorcontrib>Fiebeler, Anette</creatorcontrib><title>Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Mineralocorticoid receptor blockade protects from angiotensin II–induced target-organ damage. 11β-Hydroxysteroid dehydrogenase type 2 protects the mineralocorticoid receptor from activation by glucocorticoids; however, high glucocorticoid concentrations and absent 11β-hydroxysteroid dehydrogenase type 2 in some tissues make glucocorticoids highly relevant mineralocorticoid receptor ligands. We investigated the effects of corticosterone (10 to 10 mol/L) on early vascular mineralocorticoid receptor signaling by Western blotting, confocal microscopy, and myography. Corticosterone initiated extracellular signal–regulated kinase 1/2 phosphorylation in rat vascular smooth muscle cells at ≥10 mol/L doses. Protein synthesis inhibitors had no effect, indicating a nongenomic action. Corticosterone also stimulated c-Jun N-terminal kinase, p38, Src, and Akt phosphorylation at 15 minutes and enhanced angiotensin II–induced signaling at 5 minutes. A specific epidermal growth factor receptor blocker, AG1478, as well as the Src inhibitor PP2, markedly reduced corticosterone-induced extracellular signal–regulated kinase 1/2 phosphorylation, as did preincubation of cells with the mineralocorticoid receptor antagonist spironolactone. Silencing mineralocorticoid receptor with small interfering RNA abolished corticosterone-induced effects. Corticosterone (10 mol/L) enhanced phenylephrine-induced contraction of intact aortic rings. These effects were dependent on the intact endothelium, mineralocorticoid receptor, and mitogen-activated protein kinase kinase 1/extracellular signal-regulated kinase signaling. We conclude that corticosterone induces rapid mineralocorticoid receptor signaling in vascular smooth muscle cells that involves mitogen-activated protein kinase kinase/extracellular signal–regulated kinase–dependent pathways. These new mineralocorticoid receptor–dependent signaling pathways suggest that glucocorticoids may contribute to vascular disease via mineralocorticoid receptor signaling, independent of circulating aldosterone.</description><subject>11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism</subject><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - metabolism</subject><subject>Aorta - pathology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Corticosterone - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>MAP Kinase Kinase 1 - metabolism</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation - drug effects</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Mineralocorticoid - drug effects</subject><subject>Receptors, Mineralocorticoid - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>src-Family Kinases</subject><subject>Vasoconstriction - drug effects</subject><subject>Vertebrates: cardiovascular system</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkGFLHDEQhkOx1KvtX5BFsN_WZpLJbtZvx3H1BKvFs6V-Ctls4q3mNprsIv33TbmjhQaGMOGZd8JDyAnQM4AKPq_uvy1v75bX68ub6_lqfga0ziVqkG_IDATDEkXFD8iMQoNlA_DzkLxP6ZFSQMT6HTkEybFmHGZkdeEnE0yIY29C35W31uvRdsW6fxi074eHYumcNWMq-qH4oZOZvI7FehvCuCm-Tsl4Wyys9-kDeeu0T_bj_j4i378s7xar8urm4nIxvyoNyoqVwmDHRNd2LQMpTVWjprYVrnVcGIdVAzVS11aIQrSSMwDBRaOtqYBp2Qh-RD7tcp9jeJlsGtW2Tyb_QA82TEnlBMAGZQbPd6CJIaVonXqO_VbHXwqo-uNR_ecxv9dq5zEPH--3TO3Wdv9G9-IycLoHshPtXdSD6dNfjlHWUA4sc7jjXoMfbUxPfnq1UW2s9uNG0XyQVbJklEoqclfmYoz_Brp3jDg</recordid><startdate>200805</startdate><enddate>200805</enddate><creator>Molnar, Gergö A</creator><creator>Lindschau, Carsten</creator><creator>Dubrovska, Galyna</creator><creator>Mertens, Peter R</creator><creator>Kirsch, Torsten</creator><creator>Quinkler, Marcus</creator><creator>Gollasch, Maik</creator><creator>Wresche, Stefanie</creator><creator>Luft, Friedrich C</creator><creator>Muller, Dominik N</creator><creator>Fiebeler, Anette</creator><general>American Heart Association, Inc</general><general>Lippincott</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>7X8</scope></search><sort><creationdate>200805</creationdate><title>Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells</title><author>Molnar, Gergö A ; Lindschau, Carsten ; Dubrovska, Galyna ; Mertens, Peter R ; Kirsch, Torsten ; Quinkler, Marcus ; Gollasch, Maik ; Wresche, Stefanie ; Luft, Friedrich C ; Muller, Dominik N ; Fiebeler, Anette</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4862-5c4d25dbdb2188c674a0eb5fbf35cf4691740fb64455b832115359aec612a8953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism</topic><topic>Animals</topic><topic>Aorta - drug effects</topic><topic>Aorta - metabolism</topic><topic>Aorta - pathology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Corticosterone - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>MAP Kinase Kinase 1 - metabolism</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphorylation - drug effects</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Mineralocorticoid - drug effects</topic><topic>Receptors, Mineralocorticoid - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>src-Family Kinases</topic><topic>Vasoconstriction - drug effects</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Molnar, Gergö A</creatorcontrib><creatorcontrib>Lindschau, Carsten</creatorcontrib><creatorcontrib>Dubrovska, Galyna</creatorcontrib><creatorcontrib>Mertens, Peter R</creatorcontrib><creatorcontrib>Kirsch, Torsten</creatorcontrib><creatorcontrib>Quinkler, Marcus</creatorcontrib><creatorcontrib>Gollasch, Maik</creatorcontrib><creatorcontrib>Wresche, Stefanie</creatorcontrib><creatorcontrib>Luft, Friedrich C</creatorcontrib><creatorcontrib>Muller, Dominik N</creatorcontrib><creatorcontrib>Fiebeler, Anette</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>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Molnar, Gergö A</au><au>Lindschau, Carsten</au><au>Dubrovska, Galyna</au><au>Mertens, Peter R</au><au>Kirsch, Torsten</au><au>Quinkler, Marcus</au><au>Gollasch, Maik</au><au>Wresche, Stefanie</au><au>Luft, Friedrich C</au><au>Muller, Dominik N</au><au>Fiebeler, Anette</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2008-05</date><risdate>2008</risdate><volume>51</volume><issue>5</issue><spage>1372</spage><epage>1378</epage><pages>1372-1378</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Mineralocorticoid receptor blockade protects from angiotensin II–induced target-organ damage. 11β-Hydroxysteroid dehydrogenase type 2 protects the mineralocorticoid receptor from activation by glucocorticoids; however, high glucocorticoid concentrations and absent 11β-hydroxysteroid dehydrogenase type 2 in some tissues make glucocorticoids highly relevant mineralocorticoid receptor ligands. We investigated the effects of corticosterone (10 to 10 mol/L) on early vascular mineralocorticoid receptor signaling by Western blotting, confocal microscopy, and myography. Corticosterone initiated extracellular signal–regulated kinase 1/2 phosphorylation in rat vascular smooth muscle cells at ≥10 mol/L doses. Protein synthesis inhibitors had no effect, indicating a nongenomic action. Corticosterone also stimulated c-Jun N-terminal kinase, p38, Src, and Akt phosphorylation at 15 minutes and enhanced angiotensin II–induced signaling at 5 minutes. A specific epidermal growth factor receptor blocker, AG1478, as well as the Src inhibitor PP2, markedly reduced corticosterone-induced extracellular signal–regulated kinase 1/2 phosphorylation, as did preincubation of cells with the mineralocorticoid receptor antagonist spironolactone. Silencing mineralocorticoid receptor with small interfering RNA abolished corticosterone-induced effects. Corticosterone (10 mol/L) enhanced phenylephrine-induced contraction of intact aortic rings. These effects were dependent on the intact endothelium, mineralocorticoid receptor, and mitogen-activated protein kinase kinase 1/extracellular signal-regulated kinase signaling. We conclude that corticosterone induces rapid mineralocorticoid receptor signaling in vascular smooth muscle cells that involves mitogen-activated protein kinase kinase/extracellular signal–regulated kinase–dependent pathways. These new mineralocorticoid receptor–dependent signaling pathways suggest that glucocorticoids may contribute to vascular disease via mineralocorticoid receptor signaling, independent of circulating aldosterone.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>18347231</pmid><doi>10.1161/HYPERTENSIONAHA.107.105718</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism Animals Aorta - drug effects Aorta - metabolism Aorta - pathology Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Cardiology. Vascular system Cells, Cultured Corticosterone - pharmacology Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology JNK Mitogen-Activated Protein Kinases - metabolism MAP Kinase Kinase 1 - metabolism Medical sciences Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation - drug effects Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley Receptors, Mineralocorticoid - drug effects Receptors, Mineralocorticoid - metabolism Signal Transduction - drug effects Signal Transduction - physiology src-Family Kinases Vasoconstriction - drug effects Vertebrates: cardiovascular system |
| title | Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells |
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