Antioxidant Effect of Adrenomedullin on Angiotensin II-Induced Reactive Oxygen Species Generation in Vascular Smooth Muscle Cells
Recent adrenomedullin (AM) gene-targeting studies have proposed a novel concept that AM plays a protective role against oxidative stress in vivo. The present study was undertaken to explore the underlying molecular mechanism of the putative antioxidant action of AM against angiotensin II (Ang II)ind...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2004-07, Vol.145 (7), p.3331-3337 |
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| creator | Yoshimoto, Takanobu Fukai, Nozomi Sato, Ryuji Sugiyama, Toru Ozawa, Naoko Shichiri, Masayoshi Hirata, Yukio |
| description | Recent adrenomedullin (AM) gene-targeting studies have proposed a novel concept that AM plays a protective role against oxidative stress in vivo. The present study was undertaken to explore the underlying molecular mechanism of the putative antioxidant action of AM against angiotensin II (Ang II)induced reactive oxygen species (ROS) generation in rat vascular smooth muscle cells (VSMCs). Intracellular ROS levels were measured by dichlorofluoroscein fluorescence. Redox-sensitive c-Jun amino-terminal kinase (JNK) and ERK1/2 activation and gene expression induced by Ang II in VSMCs were also studied. AM dose-relatedly (10−8–10−7 m) inhibited intracellular ROS generation stimulated by Ang II (10−7 m), as mimicked by dibutyl-cAMP, the effect of which was inhibited by the pretreatment with N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide hydrochloride, a protein kinase A inhibitor, and calcitonin gene-related peptide(8–37), an AM/calcitonin gene-related peptide receptor antagonist. Ang II induced JNK and ERK1/2 activation via a redox-sensitive manner, whereas AM inhibited JNK, but not ERK1/2, activation by Ang II. Furthermore, AM inhibited Ang II-induced redox-sensitive gene expression (plasminogen activator inhibitor-1 and monocyte chemoattractant protein-1) in the same manner as N-acetyl-l-cysteine, a potent antioxidant. AM also inhibited Ang II-induced up-regulation of Nox1, a critical membrane-bound component of reduced nicotinamide adenine dinucleotide phosphate oxidase in VSMCs, in the same degree as N-acetyl-l-cysteine. Our study demonstrates for the first time that AM directly inhibits intracellular ROS generation via an AM receptor-mediated and c-AMP-protein kinase A-dependent mechanism in VSMCs and that AM with its potent antioxidant action inhibits redox-sensitive JNK activation and gene expression induced by Ang II. These data suggest that AM plays a protective role as an endogenous antioxidant in Ang II-induced vascular injury. |
| doi_str_mv | 10.1210/en.2003-1583 |
| format | Article |
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The present study was undertaken to explore the underlying molecular mechanism of the putative antioxidant action of AM against angiotensin II (Ang II)induced reactive oxygen species (ROS) generation in rat vascular smooth muscle cells (VSMCs). Intracellular ROS levels were measured by dichlorofluoroscein fluorescence. Redox-sensitive c-Jun amino-terminal kinase (JNK) and ERK1/2 activation and gene expression induced by Ang II in VSMCs were also studied. AM dose-relatedly (10−8–10−7 m) inhibited intracellular ROS generation stimulated by Ang II (10−7 m), as mimicked by dibutyl-cAMP, the effect of which was inhibited by the pretreatment with N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide hydrochloride, a protein kinase A inhibitor, and calcitonin gene-related peptide(8–37), an AM/calcitonin gene-related peptide receptor antagonist. Ang II induced JNK and ERK1/2 activation via a redox-sensitive manner, whereas AM inhibited JNK, but not ERK1/2, activation by Ang II. Furthermore, AM inhibited Ang II-induced redox-sensitive gene expression (plasminogen activator inhibitor-1 and monocyte chemoattractant protein-1) in the same manner as N-acetyl-l-cysteine, a potent antioxidant. AM also inhibited Ang II-induced up-regulation of Nox1, a critical membrane-bound component of reduced nicotinamide adenine dinucleotide phosphate oxidase in VSMCs, in the same degree as N-acetyl-l-cysteine. Our study demonstrates for the first time that AM directly inhibits intracellular ROS generation via an AM receptor-mediated and c-AMP-protein kinase A-dependent mechanism in VSMCs and that AM with its potent antioxidant action inhibits redox-sensitive JNK activation and gene expression induced by Ang II. These data suggest that AM plays a protective role as an endogenous antioxidant in Ang II-induced vascular injury.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2003-1583</identifier><identifier>PMID: 15070851</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Acetylcysteine ; Activation analysis ; Adenine ; Adrenomedullin ; Angiotensin ; Angiotensin II ; Angiotensin II - pharmacology ; Animals ; Antioxidants ; Antioxidants - pharmacology ; Aorta, Thoracic - cytology ; Biological and medical sciences ; Calcitonin ; Calcitonin gene-related peptide ; Cells, Cultured ; Chemokine CCL2 - genetics ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Cysteine ; Extracellular signal-regulated kinase ; Fundamental and applied biological sciences. Psychology ; Gene expression ; In vivo methods and tests ; Intracellular ; JNK Mitogen-Activated Protein Kinases ; Kinases ; Male ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases - metabolism ; Molecular modelling ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Monocytes ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; NAD(P)H oxidase ; NADH, NADPH Oxidoreductases - genetics ; NADPH Oxidase 1 ; NADPH-diaphorase ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Oxidation-Reduction ; Oxidative stress ; Oxygen ; Peptides ; Peptides - pharmacology ; Plasminogen Activator Inhibitor 1 - genetics ; Plasminogen activator inhibitors ; Protein kinase A ; Protein kinase A inhibitors ; Proteins ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptors ; Receptors, Adrenomedullin ; Receptors, Peptide - metabolism ; RNA, Messenger - analysis ; Smooth muscle ; Transcription factors ; Vasoconstrictor Agents - pharmacology ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2004-07, Vol.145 (7), p.3331-3337</ispartof><rights>Copyright © 2004 by The Endocrine Society 2004</rights><rights>2004 INIST-CNRS</rights><rights>Copyright © 2004 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-5edfe54beeaaa28345fc24aee0c6d42e3b6b689e2af0f1c0d033cef69e8ba9773</citedby><cites>FETCH-LOGICAL-c525t-5edfe54beeaaa28345fc24aee0c6d42e3b6b689e2af0f1c0d033cef69e8ba9773</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=15880306$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15070851$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshimoto, Takanobu</creatorcontrib><creatorcontrib>Fukai, Nozomi</creatorcontrib><creatorcontrib>Sato, Ryuji</creatorcontrib><creatorcontrib>Sugiyama, Toru</creatorcontrib><creatorcontrib>Ozawa, Naoko</creatorcontrib><creatorcontrib>Shichiri, Masayoshi</creatorcontrib><creatorcontrib>Hirata, Yukio</creatorcontrib><title>Antioxidant Effect of Adrenomedullin on Angiotensin II-Induced Reactive Oxygen Species Generation in Vascular Smooth Muscle Cells</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Recent adrenomedullin (AM) gene-targeting studies have proposed a novel concept that AM plays a protective role against oxidative stress in vivo. The present study was undertaken to explore the underlying molecular mechanism of the putative antioxidant action of AM against angiotensin II (Ang II)induced reactive oxygen species (ROS) generation in rat vascular smooth muscle cells (VSMCs). Intracellular ROS levels were measured by dichlorofluoroscein fluorescence. Redox-sensitive c-Jun amino-terminal kinase (JNK) and ERK1/2 activation and gene expression induced by Ang II in VSMCs were also studied. AM dose-relatedly (10−8–10−7 m) inhibited intracellular ROS generation stimulated by Ang II (10−7 m), as mimicked by dibutyl-cAMP, the effect of which was inhibited by the pretreatment with N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide hydrochloride, a protein kinase A inhibitor, and calcitonin gene-related peptide(8–37), an AM/calcitonin gene-related peptide receptor antagonist. Ang II induced JNK and ERK1/2 activation via a redox-sensitive manner, whereas AM inhibited JNK, but not ERK1/2, activation by Ang II. Furthermore, AM inhibited Ang II-induced redox-sensitive gene expression (plasminogen activator inhibitor-1 and monocyte chemoattractant protein-1) in the same manner as N-acetyl-l-cysteine, a potent antioxidant. AM also inhibited Ang II-induced up-regulation of Nox1, a critical membrane-bound component of reduced nicotinamide adenine dinucleotide phosphate oxidase in VSMCs, in the same degree as N-acetyl-l-cysteine. Our study demonstrates for the first time that AM directly inhibits intracellular ROS generation via an AM receptor-mediated and c-AMP-protein kinase A-dependent mechanism in VSMCs and that AM with its potent antioxidant action inhibits redox-sensitive JNK activation and gene expression induced by Ang II. These data suggest that AM plays a protective role as an endogenous antioxidant in Ang II-induced vascular injury.</description><subject>Acetylcysteine</subject><subject>Activation analysis</subject><subject>Adenine</subject><subject>Adrenomedullin</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Aorta, Thoracic - cytology</subject><subject>Biological and medical sciences</subject><subject>Calcitonin</subject><subject>Calcitonin gene-related peptide</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - genetics</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Cysteine</subject><subject>Extracellular signal-regulated kinase</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>In vivo methods and tests</subject><subject>Intracellular</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>Kinases</subject><subject>Male</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Molecular modelling</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>NAD(P)H oxidase</subject><subject>NADH, NADPH Oxidoreductases - genetics</subject><subject>NADPH Oxidase 1</subject><subject>NADPH-diaphorase</subject><subject>Nicotinamide</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Oxidation-Reduction</subject><subject>Oxidative stress</subject><subject>Oxygen</subject><subject>Peptides</subject><subject>Peptides - pharmacology</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Plasminogen activator inhibitors</subject><subject>Protein kinase A</subject><subject>Protein kinase A inhibitors</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors</subject><subject>Receptors, Adrenomedullin</subject><subject>Receptors, Peptide - metabolism</subject><subject>RNA, Messenger - analysis</subject><subject>Smooth muscle</subject><subject>Transcription factors</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUFr3DAQhUVpaLZpbz0XQWl7idORZNna47Ik6UJKoGl7NbI8ShW8kiPZJTnmn0fLGhJKexoGvnnzZh4h7xicMM7gC_oTDiAKJpV4QRZsWcqiZjW8JAsAJoqa8_qQvE7pJrdlWYpX5JBJqEFJtiAPKz-6cOc67Ud6ai2akQZLV11EH7bYTX3vPA2ervy1CyP6lNvNptj4bjLY0e-ozej-IL28u79GT68GNA4TPUePUWdpT_PAL53M1OtIr7YhjL_ptymZHuka-z69IQdW9wnfzvWI_Dw7_bH-Wlxcnm_Wq4vCSC7HQmJnUZYtotaaK1FKa3ipEcFUXclRtFVbqSVybcEyAx0IYdBWS1StXta1OCKf9rpDDLcTprHZumSyA-0xTKmpOfCKc8jgh7_AmzBFn701ggmQChTs5I73lIkhpYi2GaLb6njfMGh2wTTom10wzS6YjL-fRac2v_UJnpPIwMcZyL_SvY3aG5eecUqBgCpzn_dcmIb_rSzmlWJPou-Cic7jEDGlp2v-afQRE9-0XA</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>Yoshimoto, Takanobu</creator><creator>Fukai, Nozomi</creator><creator>Sato, Ryuji</creator><creator>Sugiyama, Toru</creator><creator>Ozawa, Naoko</creator><creator>Shichiri, Masayoshi</creator><creator>Hirata, Yukio</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20040701</creationdate><title>Antioxidant Effect of Adrenomedullin on Angiotensin II-Induced Reactive Oxygen Species Generation in Vascular Smooth Muscle Cells</title><author>Yoshimoto, Takanobu ; Fukai, Nozomi ; Sato, Ryuji ; Sugiyama, Toru ; Ozawa, Naoko ; Shichiri, Masayoshi ; Hirata, Yukio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-5edfe54beeaaa28345fc24aee0c6d42e3b6b689e2af0f1c0d033cef69e8ba9773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acetylcysteine</topic><topic>Activation analysis</topic><topic>Adenine</topic><topic>Adrenomedullin</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Aorta, Thoracic - cytology</topic><topic>Biological and medical sciences</topic><topic>Calcitonin</topic><topic>Calcitonin gene-related peptide</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - genetics</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Cysteine</topic><topic>Extracellular signal-regulated kinase</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>In vivo methods and tests</topic><topic>Intracellular</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>Kinases</topic><topic>Male</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Molecular modelling</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>NAD(P)H oxidase</topic><topic>NADH, NADPH Oxidoreductases - genetics</topic><topic>NADPH Oxidase 1</topic><topic>NADPH-diaphorase</topic><topic>Nicotinamide</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Oxidation-Reduction</topic><topic>Oxidative stress</topic><topic>Oxygen</topic><topic>Peptides</topic><topic>Peptides - pharmacology</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Plasminogen activator inhibitors</topic><topic>Protein kinase A</topic><topic>Protein kinase A inhibitors</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors</topic><topic>Receptors, Adrenomedullin</topic><topic>Receptors, Peptide - metabolism</topic><topic>RNA, Messenger - analysis</topic><topic>Smooth muscle</topic><topic>Transcription factors</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshimoto, Takanobu</creatorcontrib><creatorcontrib>Fukai, Nozomi</creatorcontrib><creatorcontrib>Sato, Ryuji</creatorcontrib><creatorcontrib>Sugiyama, Toru</creatorcontrib><creatorcontrib>Ozawa, Naoko</creatorcontrib><creatorcontrib>Shichiri, Masayoshi</creatorcontrib><creatorcontrib>Hirata, Yukio</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>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshimoto, Takanobu</au><au>Fukai, Nozomi</au><au>Sato, Ryuji</au><au>Sugiyama, Toru</au><au>Ozawa, Naoko</au><au>Shichiri, Masayoshi</au><au>Hirata, Yukio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antioxidant Effect of Adrenomedullin on Angiotensin II-Induced Reactive Oxygen Species Generation in Vascular Smooth Muscle Cells</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2004-07-01</date><risdate>2004</risdate><volume>145</volume><issue>7</issue><spage>3331</spage><epage>3337</epage><pages>3331-3337</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Recent adrenomedullin (AM) gene-targeting studies have proposed a novel concept that AM plays a protective role against oxidative stress in vivo. The present study was undertaken to explore the underlying molecular mechanism of the putative antioxidant action of AM against angiotensin II (Ang II)induced reactive oxygen species (ROS) generation in rat vascular smooth muscle cells (VSMCs). Intracellular ROS levels were measured by dichlorofluoroscein fluorescence. Redox-sensitive c-Jun amino-terminal kinase (JNK) and ERK1/2 activation and gene expression induced by Ang II in VSMCs were also studied. AM dose-relatedly (10−8–10−7 m) inhibited intracellular ROS generation stimulated by Ang II (10−7 m), as mimicked by dibutyl-cAMP, the effect of which was inhibited by the pretreatment with N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide hydrochloride, a protein kinase A inhibitor, and calcitonin gene-related peptide(8–37), an AM/calcitonin gene-related peptide receptor antagonist. Ang II induced JNK and ERK1/2 activation via a redox-sensitive manner, whereas AM inhibited JNK, but not ERK1/2, activation by Ang II. Furthermore, AM inhibited Ang II-induced redox-sensitive gene expression (plasminogen activator inhibitor-1 and monocyte chemoattractant protein-1) in the same manner as N-acetyl-l-cysteine, a potent antioxidant. AM also inhibited Ang II-induced up-regulation of Nox1, a critical membrane-bound component of reduced nicotinamide adenine dinucleotide phosphate oxidase in VSMCs, in the same degree as N-acetyl-l-cysteine. Our study demonstrates for the first time that AM directly inhibits intracellular ROS generation via an AM receptor-mediated and c-AMP-protein kinase A-dependent mechanism in VSMCs and that AM with its potent antioxidant action inhibits redox-sensitive JNK activation and gene expression induced by Ang II. These data suggest that AM plays a protective role as an endogenous antioxidant in Ang II-induced vascular injury.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>15070851</pmid><doi>10.1210/en.2003-1583</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Endocrinology (Philadelphia), 2004-07, Vol.145 (7), p.3331-3337 |
| issn | 0013-7227 1945-7170 |
| language | eng |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Acetylcysteine Activation analysis Adenine Adrenomedullin Angiotensin Angiotensin II Angiotensin II - pharmacology Animals Antioxidants Antioxidants - pharmacology Aorta, Thoracic - cytology Biological and medical sciences Calcitonin Calcitonin gene-related peptide Cells, Cultured Chemokine CCL2 - genetics Cyclic AMP-Dependent Protein Kinases - metabolism Cysteine Extracellular signal-regulated kinase Fundamental and applied biological sciences. Psychology Gene expression In vivo methods and tests Intracellular JNK Mitogen-Activated Protein Kinases Kinases Male Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases - metabolism Molecular modelling Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism NAD(P)H oxidase NADH, NADPH Oxidoreductases - genetics NADPH Oxidase 1 NADPH-diaphorase Nicotinamide Nicotinamide adenine dinucleotide Oxidation-Reduction Oxidative stress Oxygen Peptides Peptides - pharmacology Plasminogen Activator Inhibitor 1 - genetics Plasminogen activator inhibitors Protein kinase A Protein kinase A inhibitors Proteins Rats Rats, Sprague-Dawley Reactive oxygen species Reactive Oxygen Species - metabolism Receptors Receptors, Adrenomedullin Receptors, Peptide - metabolism RNA, Messenger - analysis Smooth muscle Transcription factors Vasoconstrictor Agents - pharmacology Vertebrates: endocrinology |
| title | Antioxidant Effect of Adrenomedullin on Angiotensin II-Induced Reactive Oxygen Species Generation in Vascular Smooth Muscle Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T19%3A12%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Antioxidant%20Effect%20of%20Adrenomedullin%20on%20Angiotensin%20II-Induced%20Reactive%20Oxygen%20Species%20Generation%20in%20Vascular%20Smooth%20Muscle%20Cells&rft.jtitle=Endocrinology%20(Philadelphia)&rft.au=Yoshimoto,%20Takanobu&rft.date=2004-07-01&rft.volume=145&rft.issue=7&rft.spage=3331&rft.epage=3337&rft.pages=3331-3337&rft.issn=0013-7227&rft.eissn=1945-7170&rft.coden=ENDOAO&rft_id=info:doi/10.1210/en.2003-1583&rft_dat=%3Cproquest_cross%3E3130580807%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3130580807&rft_id=info:pmid/15070851&rft_oup_id=10.1210/en.2003-1583&rfr_iscdi=true |