Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways
BACKGROUND—Carbon monoxide (CO) is postulated to protect tissues against several types of injuries. We investigated the role of CO in amelioration of cardiac ischemia–reperfusion injury in vivo and the mechanisms involved in it. METHODS AND RESULTS—Rats inhaled CO (250 ppm, 500 ppm, or 1000 ppm) for...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-10, Vol.24 (10), p.1848-1853 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Fujimoto, Hajime Ohno, Minoru Ayabe, Seiji Kobayashi, Hisae Ishizaka, Nobukazu Kimura, Hiroko Yoshida, Ken-ichi Nagai, Ryozo |
| description | BACKGROUND—Carbon monoxide (CO) is postulated to protect tissues against several types of injuries. We investigated the role of CO in amelioration of cardiac ischemia–reperfusion injury in vivo and the mechanisms involved in it.
METHODS AND RESULTS—Rats inhaled CO (250 ppm, 500 ppm, or 1000 ppm) for 24 hours in a chamber after myocardial ischemia–reperfusion induced by occluding the left anterior descending coronary artery for 30 minutes. Pre-exposure to 1000 ppm of CO significantly reduced the ratio of infarct areas to risk areas and suppressed the migration of macrophages and monocytes into infarct areas, and the expression of tumor necrosis factor (TNF)-α in the heart; however, 250 ppm, 500 ppm of CO, or low barometric pressure hypoxia (0.5 atm) did not affect them. Exposure to 1000 ppm CO resulted in the activation of p38 mitogen-activated protein kinase (p38MAPK), protein kinase Bα(Akt), endothelial nitric oxide synthase (eNOS), and cyclic guanosine monophosphate (cGMP) in the myocardium. Inhibition of p38MAPK, PI3kinase, NO, and soluble guanylate cyclase with SB203580, wortmannin, N(G)-nitro-l-arginine methyl ester (l-NAME), and methylene blue, respectively, attenuated the cytoprotection by CO.
CONCLUSION—CO has beneficial effects on cardiac ischemia–reperfusion injury; this effect is mediated by p38MAPK pathway and Akt–eNOS pathway, including production of cGMP. |
| doi_str_mv | 10.1161/01.ATV.0000142364.85911.0e |
| format | Article |
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METHODS AND RESULTS—Rats inhaled CO (250 ppm, 500 ppm, or 1000 ppm) for 24 hours in a chamber after myocardial ischemia–reperfusion induced by occluding the left anterior descending coronary artery for 30 minutes. Pre-exposure to 1000 ppm of CO significantly reduced the ratio of infarct areas to risk areas and suppressed the migration of macrophages and monocytes into infarct areas, and the expression of tumor necrosis factor (TNF)-α in the heart; however, 250 ppm, 500 ppm of CO, or low barometric pressure hypoxia (0.5 atm) did not affect them. Exposure to 1000 ppm CO resulted in the activation of p38 mitogen-activated protein kinase (p38MAPK), protein kinase Bα(Akt), endothelial nitric oxide synthase (eNOS), and cyclic guanosine monophosphate (cGMP) in the myocardium. Inhibition of p38MAPK, PI3kinase, NO, and soluble guanylate cyclase with SB203580, wortmannin, N(G)-nitro-l-arginine methyl ester (l-NAME), and methylene blue, respectively, attenuated the cytoprotection by CO.
CONCLUSION—CO has beneficial effects on cardiac ischemia–reperfusion injury; this effect is mediated by p38MAPK pathway and Akt–eNOS pathway, including production of cGMP.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000142364.85911.0e</identifier><identifier>PMID: 15308554</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Carbon Monoxide - metabolism ; Carbon Monoxide - pharmacology ; Cardiology. Vascular system ; Cardiovascular system ; Cyclic GMP - physiology ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Hemoglobins - metabolism ; Inhalation - physiology ; Medical sciences ; Mitogen-Activated Protein Kinases - metabolism ; Myocardial Ischemia - prevention & control ; Myocardium - enzymology ; Myocardium - metabolism ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type III ; Pharmacology. Drug treatments ; Protein-Serine-Threonine Kinases - metabolism ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Reperfusion Injury - prevention & control ; Tumor Necrosis Factor-alpha - biosynthesis ; Vasodilator agents. Cerebral vasodilators</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-10, Vol.24 (10), p.1848-1853</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5439-9390d9efb5c68911fc00319c603b0cd86782c968ee5e228b6a7d3a014bbc70403</citedby><cites>FETCH-LOGICAL-c5439-9390d9efb5c68911fc00319c603b0cd86782c968ee5e228b6a7d3a014bbc70403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16185721$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15308554$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fujimoto, Hajime</creatorcontrib><creatorcontrib>Ohno, Minoru</creatorcontrib><creatorcontrib>Ayabe, Seiji</creatorcontrib><creatorcontrib>Kobayashi, Hisae</creatorcontrib><creatorcontrib>Ishizaka, Nobukazu</creatorcontrib><creatorcontrib>Kimura, Hiroko</creatorcontrib><creatorcontrib>Yoshida, Ken-ichi</creatorcontrib><creatorcontrib>Nagai, Ryozo</creatorcontrib><title>Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>BACKGROUND—Carbon monoxide (CO) is postulated to protect tissues against several types of injuries. We investigated the role of CO in amelioration of cardiac ischemia–reperfusion injury in vivo and the mechanisms involved in it.
METHODS AND RESULTS—Rats inhaled CO (250 ppm, 500 ppm, or 1000 ppm) for 24 hours in a chamber after myocardial ischemia–reperfusion induced by occluding the left anterior descending coronary artery for 30 minutes. Pre-exposure to 1000 ppm of CO significantly reduced the ratio of infarct areas to risk areas and suppressed the migration of macrophages and monocytes into infarct areas, and the expression of tumor necrosis factor (TNF)-α in the heart; however, 250 ppm, 500 ppm of CO, or low barometric pressure hypoxia (0.5 atm) did not affect them. Exposure to 1000 ppm CO resulted in the activation of p38 mitogen-activated protein kinase (p38MAPK), protein kinase Bα(Akt), endothelial nitric oxide synthase (eNOS), and cyclic guanosine monophosphate (cGMP) in the myocardium. Inhibition of p38MAPK, PI3kinase, NO, and soluble guanylate cyclase with SB203580, wortmannin, N(G)-nitro-l-arginine methyl ester (l-NAME), and methylene blue, respectively, attenuated the cytoprotection by CO.
CONCLUSION—CO has beneficial effects on cardiac ischemia–reperfusion injury; this effect is mediated by p38MAPK pathway and Akt–eNOS pathway, including production of cGMP.</description><subject>Animals</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Carbon Monoxide - metabolism</subject><subject>Carbon Monoxide - pharmacology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular system</subject><subject>Cyclic GMP - physiology</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Hemoglobins - metabolism</subject><subject>Inhalation - physiology</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Myocardial Ischemia - prevention & control</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Pharmacology. Drug treatments</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Rats</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Vasodilator agents. Cerebral vasodilators</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN1u0zAUxyPExMbgFZCFBHcJ_k7MXVTxUW1jFYzdWo5zQr2lcbGTld7xEDzhngR3rVRL1jkXv7_P8S_L3hJcECLJB0yK-ua2wOkQTpnkRSUUIQWGZ9kZEZTnXDL5PPW4VLmQnJ5mL2O8SzynFL_ITolguBKCn2V-ZkLjB3TlB__HtYAWwY9gx4jqX8YNcUQJaJ2xaB7tElbOPP799x3WELopuhScD3dT2KaCbt2DRw_OoKt6cYHM0KL6fkw0fLv-gRZmXG7MNr7KTjrTR3h9qOfZz8-fbmZf88vrL_NZfZlbwZnKFVO4VdA1wsoq_a2zGDOirMSswbatZFlRq2QFIIDSqpGmbJlJOprGlphjdp6937-7Dv73BHHUKxct9L0ZwE9RS6lEujSBH_egDT7GAJ1eB7cyYasJ1jvdGhOddOujbv2kW2NI4TeHKVOzgvYYPfhNwLsDYKI1fRfMYF08cpJUoqQkcXzPbXw_Qoj3_bSBoJdg-nG5G82ZxCKnqSG7RfLdMor9B6cumaI</recordid><startdate>200410</startdate><enddate>200410</enddate><creator>Fujimoto, Hajime</creator><creator>Ohno, Minoru</creator><creator>Ayabe, Seiji</creator><creator>Kobayashi, Hisae</creator><creator>Ishizaka, Nobukazu</creator><creator>Kimura, Hiroko</creator><creator>Yoshida, Ken-ichi</creator><creator>Nagai, Ryozo</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>200410</creationdate><title>Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways</title><author>Fujimoto, Hajime ; Ohno, Minoru ; Ayabe, Seiji ; Kobayashi, Hisae ; Ishizaka, Nobukazu ; Kimura, Hiroko ; Yoshida, Ken-ichi ; Nagai, Ryozo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5439-9390d9efb5c68911fc00319c603b0cd86782c968ee5e228b6a7d3a014bbc70403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Carbon Monoxide - metabolism</topic><topic>Carbon Monoxide - pharmacology</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular system</topic><topic>Cyclic GMP - physiology</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Hemoglobins - metabolism</topic><topic>Inhalation - physiology</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Myocardial Ischemia - prevention & control</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Pharmacology. Drug treatments</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Rats</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Vasodilator agents. Cerebral vasodilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujimoto, Hajime</creatorcontrib><creatorcontrib>Ohno, Minoru</creatorcontrib><creatorcontrib>Ayabe, Seiji</creatorcontrib><creatorcontrib>Kobayashi, Hisae</creatorcontrib><creatorcontrib>Ishizaka, Nobukazu</creatorcontrib><creatorcontrib>Kimura, Hiroko</creatorcontrib><creatorcontrib>Yoshida, Ken-ichi</creatorcontrib><creatorcontrib>Nagai, Ryozo</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>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujimoto, Hajime</au><au>Ohno, Minoru</au><au>Ayabe, Seiji</au><au>Kobayashi, Hisae</au><au>Ishizaka, Nobukazu</au><au>Kimura, Hiroko</au><au>Yoshida, Ken-ichi</au><au>Nagai, Ryozo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-10</date><risdate>2004</risdate><volume>24</volume><issue>10</issue><spage>1848</spage><epage>1853</epage><pages>1848-1853</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>BACKGROUND—Carbon monoxide (CO) is postulated to protect tissues against several types of injuries. We investigated the role of CO in amelioration of cardiac ischemia–reperfusion injury in vivo and the mechanisms involved in it.
METHODS AND RESULTS—Rats inhaled CO (250 ppm, 500 ppm, or 1000 ppm) for 24 hours in a chamber after myocardial ischemia–reperfusion induced by occluding the left anterior descending coronary artery for 30 minutes. Pre-exposure to 1000 ppm of CO significantly reduced the ratio of infarct areas to risk areas and suppressed the migration of macrophages and monocytes into infarct areas, and the expression of tumor necrosis factor (TNF)-α in the heart; however, 250 ppm, 500 ppm of CO, or low barometric pressure hypoxia (0.5 atm) did not affect them. Exposure to 1000 ppm CO resulted in the activation of p38 mitogen-activated protein kinase (p38MAPK), protein kinase Bα(Akt), endothelial nitric oxide synthase (eNOS), and cyclic guanosine monophosphate (cGMP) in the myocardium. Inhibition of p38MAPK, PI3kinase, NO, and soluble guanylate cyclase with SB203580, wortmannin, N(G)-nitro-l-arginine methyl ester (l-NAME), and methylene blue, respectively, attenuated the cytoprotection by CO.
CONCLUSION—CO has beneficial effects on cardiac ischemia–reperfusion injury; this effect is mediated by p38MAPK pathway and Akt–eNOS pathway, including production of cGMP.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15308554</pmid><doi>10.1161/01.ATV.0000142364.85911.0e</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Carbon Monoxide - metabolism Carbon Monoxide - pharmacology Cardiology. Vascular system Cardiovascular system Cyclic GMP - physiology Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Hemoglobins - metabolism Inhalation - physiology Medical sciences Mitogen-Activated Protein Kinases - metabolism Myocardial Ischemia - prevention & control Myocardium - enzymology Myocardium - metabolism Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type III Pharmacology. Drug treatments Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt Rats Reperfusion Injury - prevention & control Tumor Necrosis Factor-alpha - biosynthesis Vasodilator agents. Cerebral vasodilators |
| title | Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways |
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