β-Adrenergic Receptor–Stimulated Apoptosis in Cardiac Myocytes Is Mediated by Reactive Oxygen Species/c-Jun NH2-Terminal Kinase–Dependent Activation of the Mitochondrial Pathway
Stimulation of β-adrenergic receptors (βARs) causes apoptosis in adult rat ventricular myocytes (ARVMs). The role of reactive oxygen species (ROS) in mediating βAR-stimulated apoptosis is not known. Stimulation of βARs with norepinephrine (10 μmol/L) in the presence of prazosin (100 nmol/L) for 24 h...
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| Veröffentlicht in: | Circulation research 2003-02, Vol.92 (2), p.136-138 |
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| creator | Remondino, Andrea Kwon, Susan H Communal, Catherine Pimentel, David R Sawyer, Douglas B Singh, Krishna Colucci, Wilson S |
| description | Stimulation of β-adrenergic receptors (βARs) causes apoptosis in adult rat ventricular myocytes (ARVMs). The role of reactive oxygen species (ROS) in mediating βAR-stimulated apoptosis is not known. Stimulation of βARs with norepinephrine (10 μmol/L) in the presence of prazosin (100 nmol/L) for 24 hours increased the number of apoptotic myocytes as determined by TUNEL staining by 3.6- fold. The superoxide dismutase/catalase mimetics Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 10 μmol/L) and Euk-134 decreased βAR-stimulated apoptosis by 89±6% and 76±10%, respectively. Infection with an adenovirus expressing catalase decreased βAR-stimulated apoptosis by 82±15%. The mitochondrial permeability transition pore inhibitor bongkrekic acid (50 μmol/L) decreased βAR-stimulated apoptosis by 76±8%, and the caspase inhibitor zVAD-fmk (25 μmol/L) decreased βAR-stimulated apoptosis by 62±11%. βAR-stimulated cytochrome c release was inhibited by MnTMPyP. βAR stimulation caused c-Jun NH2-terminal kinase (JNK) activation, which was abolished by MnTMPyP. Transfection with an adenovirus expressing dominant-negative JNK inhibited βAR-stimulated apoptosis by 81±12%, and the JNK inhibitor SP600125 inhibited both βAR-stimulated apoptosis and cytochrome c release. Thus, βAR-stimulated apoptosis in ARVMs involves ROS/JNK-dependent activation of the mitochondrial death pathway. |
| doi_str_mv | 10.1161/01.RES.0000054624.03539.B4 |
| format | Article |
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The role of reactive oxygen species (ROS) in mediating βAR-stimulated apoptosis is not known. Stimulation of βARs with norepinephrine (10 μmol/L) in the presence of prazosin (100 nmol/L) for 24 hours increased the number of apoptotic myocytes as determined by TUNEL staining by 3.6- fold. The superoxide dismutase/catalase mimetics Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 10 μmol/L) and Euk-134 decreased βAR-stimulated apoptosis by 89±6% and 76±10%, respectively. Infection with an adenovirus expressing catalase decreased βAR-stimulated apoptosis by 82±15%. The mitochondrial permeability transition pore inhibitor bongkrekic acid (50 μmol/L) decreased βAR-stimulated apoptosis by 76±8%, and the caspase inhibitor zVAD-fmk (25 μmol/L) decreased βAR-stimulated apoptosis by 62±11%. βAR-stimulated cytochrome c release was inhibited by MnTMPyP. βAR stimulation caused c-Jun NH2-terminal kinase (JNK) activation, which was abolished by MnTMPyP. Transfection with an adenovirus expressing dominant-negative JNK inhibited βAR-stimulated apoptosis by 81±12%, and the JNK inhibitor SP600125 inhibited both βAR-stimulated apoptosis and cytochrome c release. Thus, βAR-stimulated apoptosis in ARVMs involves ROS/JNK-dependent activation of the mitochondrial death pathway.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000054624.03539.B4</identifier><identifier>PMID: 12574140</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Bongkrekic Acid - pharmacology ; Caspase Inhibitors ; Catalase - biosynthesis ; Catalase - genetics ; Catalase - pharmacology ; Cells, Cultured ; Cytochrome c Group - metabolism ; Enzyme Inhibitors - pharmacology ; Free Radical Scavengers - pharmacology ; Fundamental and applied biological sciences. Psychology ; Heart ; Ion Channels - antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases ; Metalloporphyrins - pharmacology ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial Membrane Transport Proteins ; Mitogen-Activated Protein Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinases - genetics ; Mitogen-Activated Protein Kinases - metabolism ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - metabolism ; Norepinephrine - pharmacology ; Organometallic Compounds - pharmacology ; Prazosin - pharmacology ; Rats ; Reactive Oxygen Species - metabolism ; Receptors, Adrenergic, beta - drug effects ; Receptors, Adrenergic, beta - metabolism ; Salicylates - pharmacology ; Signal Transduction - physiology ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 2003-02, Vol.92 (2), p.136-138</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Feb 7 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14562368$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12574140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Remondino, Andrea</creatorcontrib><creatorcontrib>Kwon, Susan H</creatorcontrib><creatorcontrib>Communal, Catherine</creatorcontrib><creatorcontrib>Pimentel, David R</creatorcontrib><creatorcontrib>Sawyer, Douglas B</creatorcontrib><creatorcontrib>Singh, Krishna</creatorcontrib><creatorcontrib>Colucci, Wilson S</creatorcontrib><title>β-Adrenergic Receptor–Stimulated Apoptosis in Cardiac Myocytes Is Mediated by Reactive Oxygen Species/c-Jun NH2-Terminal Kinase–Dependent Activation of the Mitochondrial Pathway</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Stimulation of β-adrenergic receptors (βARs) causes apoptosis in adult rat ventricular myocytes (ARVMs). The role of reactive oxygen species (ROS) in mediating βAR-stimulated apoptosis is not known. Stimulation of βARs with norepinephrine (10 μmol/L) in the presence of prazosin (100 nmol/L) for 24 hours increased the number of apoptotic myocytes as determined by TUNEL staining by 3.6- fold. The superoxide dismutase/catalase mimetics Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 10 μmol/L) and Euk-134 decreased βAR-stimulated apoptosis by 89±6% and 76±10%, respectively. Infection with an adenovirus expressing catalase decreased βAR-stimulated apoptosis by 82±15%. The mitochondrial permeability transition pore inhibitor bongkrekic acid (50 μmol/L) decreased βAR-stimulated apoptosis by 76±8%, and the caspase inhibitor zVAD-fmk (25 μmol/L) decreased βAR-stimulated apoptosis by 62±11%. βAR-stimulated cytochrome c release was inhibited by MnTMPyP. βAR stimulation caused c-Jun NH2-terminal kinase (JNK) activation, which was abolished by MnTMPyP. Transfection with an adenovirus expressing dominant-negative JNK inhibited βAR-stimulated apoptosis by 81±12%, and the JNK inhibitor SP600125 inhibited both βAR-stimulated apoptosis and cytochrome c release. Thus, βAR-stimulated apoptosis in ARVMs involves ROS/JNK-dependent activation of the mitochondrial death pathway.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Bongkrekic Acid - pharmacology</subject><subject>Caspase Inhibitors</subject><subject>Catalase - biosynthesis</subject><subject>Catalase - genetics</subject><subject>Catalase - pharmacology</subject><subject>Cells, Cultured</subject><subject>Cytochrome c Group - metabolism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Ion Channels - antagonists & inhibitors</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>Metalloporphyrins - pharmacology</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Membrane Transport Proteins</subject><subject>Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinases - genetics</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Norepinephrine - pharmacology</subject><subject>Organometallic Compounds - pharmacology</subject><subject>Prazosin - pharmacology</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Adrenergic, beta - drug effects</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Salicylates - pharmacology</subject><subject>Signal Transduction - physiology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdks9u1DAQxiMEoqXwCsiqBLds_S_x5rgshRa6FHXLOXLsSdcla6e2w5Ib78CbcOAxeAieBEddhIQPHumb38xoPjvLjgmeEVKSE0xmV6frGZ5OwUvKZ5gVrJq94g-yQ1JQnvNCkIfZYcpXuWAMH2RPQrjFmHBGq8fZAaGF4ITjw-znrx_5Qnuw4G-MQlegoI_O__72fR3NduhkBI0WvUtiMAEZi5bSayMVWo1OjRECOg9oBUmayGZMLaSK5gugy6_jDVi07kEZCCcqfzdY9OGM5tfgt8bKDr1Pd4A06zX0YDXYiBZTrYzGWeRaFDeAViY6tXFWe5NKPsq42cnxafaolV2AZ_t4lH16c3q9PMsvLt-eLxcXec9wJfJWYaC8nGPRUpg3DZYUgFacaowbrVnLGqoKgCr5SBqRDFKlahpRSCaobjU7yl7e9-29uxsgxHprgoKukxbcEGrBMJ7PWZnA4__AWzf4tGSoKaHJdkpYgp7voaHZgq57b7bSj_Xf50jAiz0gg5Jd66VVJvzjeFFSVs4Tx--5nesi-PC5G3bg6w3ILm7q6V8wTGhOp0ixwPkkCfYHygawHg</recordid><startdate>20030207</startdate><enddate>20030207</enddate><creator>Remondino, Andrea</creator><creator>Kwon, Susan H</creator><creator>Communal, Catherine</creator><creator>Pimentel, David R</creator><creator>Sawyer, Douglas B</creator><creator>Singh, Krishna</creator><creator>Colucci, Wilson S</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams & Wilkins Ovid Technologies</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20030207</creationdate><title>β-Adrenergic Receptor–Stimulated Apoptosis in Cardiac Myocytes Is Mediated by Reactive Oxygen Species/c-Jun NH2-Terminal Kinase–Dependent Activation of the Mitochondrial Pathway</title><author>Remondino, Andrea ; Kwon, Susan H ; Communal, Catherine ; Pimentel, David R ; Sawyer, Douglas B ; Singh, Krishna ; Colucci, Wilson S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p3097-fc0e246807f2e8bb0a2ee2942d00bdd3f3b2c5ee90541b7001c6cbb75a372dfd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Bongkrekic Acid - pharmacology</topic><topic>Caspase Inhibitors</topic><topic>Catalase - biosynthesis</topic><topic>Catalase - genetics</topic><topic>Catalase - pharmacology</topic><topic>Cells, Cultured</topic><topic>Cytochrome c Group - metabolism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Ion Channels - antagonists & inhibitors</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>Metalloporphyrins - pharmacology</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial Membrane Transport Proteins</topic><topic>Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinases - genetics</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Norepinephrine - pharmacology</topic><topic>Organometallic Compounds - pharmacology</topic><topic>Prazosin - pharmacology</topic><topic>Rats</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, Adrenergic, beta - drug effects</topic><topic>Receptors, Adrenergic, beta - metabolism</topic><topic>Salicylates - pharmacology</topic><topic>Signal Transduction - physiology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Remondino, Andrea</creatorcontrib><creatorcontrib>Kwon, Susan H</creatorcontrib><creatorcontrib>Communal, Catherine</creatorcontrib><creatorcontrib>Pimentel, David R</creatorcontrib><creatorcontrib>Sawyer, Douglas B</creatorcontrib><creatorcontrib>Singh, Krishna</creatorcontrib><creatorcontrib>Colucci, Wilson S</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Remondino, Andrea</au><au>Kwon, Susan H</au><au>Communal, Catherine</au><au>Pimentel, David R</au><au>Sawyer, Douglas B</au><au>Singh, Krishna</au><au>Colucci, Wilson S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>β-Adrenergic Receptor–Stimulated Apoptosis in Cardiac Myocytes Is Mediated by Reactive Oxygen Species/c-Jun NH2-Terminal Kinase–Dependent Activation of the Mitochondrial Pathway</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2003-02-07</date><risdate>2003</risdate><volume>92</volume><issue>2</issue><spage>136</spage><epage>138</epage><pages>136-138</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Stimulation of β-adrenergic receptors (βARs) causes apoptosis in adult rat ventricular myocytes (ARVMs). The role of reactive oxygen species (ROS) in mediating βAR-stimulated apoptosis is not known. Stimulation of βARs with norepinephrine (10 μmol/L) in the presence of prazosin (100 nmol/L) for 24 hours increased the number of apoptotic myocytes as determined by TUNEL staining by 3.6- fold. The superoxide dismutase/catalase mimetics Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (MnTMPyP; 10 μmol/L) and Euk-134 decreased βAR-stimulated apoptosis by 89±6% and 76±10%, respectively. Infection with an adenovirus expressing catalase decreased βAR-stimulated apoptosis by 82±15%. The mitochondrial permeability transition pore inhibitor bongkrekic acid (50 μmol/L) decreased βAR-stimulated apoptosis by 76±8%, and the caspase inhibitor zVAD-fmk (25 μmol/L) decreased βAR-stimulated apoptosis by 62±11%. βAR-stimulated cytochrome c release was inhibited by MnTMPyP. βAR stimulation caused c-Jun NH2-terminal kinase (JNK) activation, which was abolished by MnTMPyP. Transfection with an adenovirus expressing dominant-negative JNK inhibited βAR-stimulated apoptosis by 81±12%, and the JNK inhibitor SP600125 inhibited both βAR-stimulated apoptosis and cytochrome c release. Thus, βAR-stimulated apoptosis in ARVMs involves ROS/JNK-dependent activation of the mitochondrial death pathway.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12574140</pmid><doi>10.1161/01.RES.0000054624.03539.B4</doi><tpages>3</tpages></addata></record> |
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| ispartof | Circulation research, 2003-02, Vol.92 (2), p.136-138 |
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| source | MEDLINE; American Heart Association; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Bongkrekic Acid - pharmacology Caspase Inhibitors Catalase - biosynthesis Catalase - genetics Catalase - pharmacology Cells, Cultured Cytochrome c Group - metabolism Enzyme Inhibitors - pharmacology Free Radical Scavengers - pharmacology Fundamental and applied biological sciences. Psychology Heart Ion Channels - antagonists & inhibitors JNK Mitogen-Activated Protein Kinases Metalloporphyrins - pharmacology Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Membrane Transport Proteins Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - genetics Mitogen-Activated Protein Kinases - metabolism Myocytes, Cardiac - cytology Myocytes, Cardiac - metabolism Norepinephrine - pharmacology Organometallic Compounds - pharmacology Prazosin - pharmacology Rats Reactive Oxygen Species - metabolism Receptors, Adrenergic, beta - drug effects Receptors, Adrenergic, beta - metabolism Salicylates - pharmacology Signal Transduction - physiology Vertebrates: cardiovascular system |
| title | β-Adrenergic Receptor–Stimulated Apoptosis in Cardiac Myocytes Is Mediated by Reactive Oxygen Species/c-Jun NH2-Terminal Kinase–Dependent Activation of the Mitochondrial Pathway |
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