Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats
Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats Satoshi Imaizumi, Shin-ichiro Miura, Kazuto Nakamura, Yoshihiro Kiya, Yoshinari Uehara, Bo Zhang, Yoshino Matsuo, Hidenori Urata, Munehito Ideishi, Kerry-Anne Rye, Masataka Sata, Keijiro Saku We...
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creator | Imaizumi, Satoshi, MD Miura, Shin-ichiro, MD, PhD Nakamura, Kazuto, MD, PhD Kiya, Yoshihiro, MD Uehara, Yoshinari, MD, PhD Zhang, Bo, PhD Matsuo, Yoshino, PhD Urata, Hidenori, MD, PhD Ideishi, Munehito, MD, PhD Rye, Kerry-Anne, PhD Sata, Masataka, MD, PhD Saku, Keijiro, MD, PhD, FACC |
description | Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats Satoshi Imaizumi, Shin-ichiro Miura, Kazuto Nakamura, Yoshihiro Kiya, Yoshinari Uehara, Bo Zhang, Yoshino Matsuo, Hidenori Urata, Munehito Ideishi, Kerry-Anne Rye, Masataka Sata, Keijiro Saku We analyzed the suppression of reperfusion-induced arrhythmias by reconstituted high-density lipoprotein (rHDL) in rats. Ventricular arrhythmias after reperfusion in rHDL–pre-treated rats were significantly suppressed. This effect was mediated by an Akt protein kinase/extracellular-signal-regulated kinase (ERK)/endothelial nitric oxide (NO) synthesis pathway. We also found that rHDL activated Akt/ERK/NO in human coronary artery endothelial cells. In addition, rHDL activated ERK in adenosine triphosphate-binding cassette transporter A1- or G1-transfected but not scavenger receptor class B, type I–transfected ldlA7 cells. Therefore, rHDL-induced NO production, probably through an Akt/ERK/NO pathway in endothelial cells, may induce an antiarrhythmogenic effect. The HDL-based therapy may hold the promise of reducing the incidence of such arrhythmias after ischemia/reperfusion. |
doi_str_mv | 10.1016/j.jacc.2007.12.040 |
format | Article |
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Ventricular arrhythmias after reperfusion in rHDL–pre-treated rats were significantly suppressed. This effect was mediated by an Akt protein kinase/extracellular-signal-regulated kinase (ERK)/endothelial nitric oxide (NO) synthesis pathway. We also found that rHDL activated Akt/ERK/NO in human coronary artery endothelial cells. In addition, rHDL activated ERK in adenosine triphosphate-binding cassette transporter A1- or G1-transfected but not scavenger receptor class B, type I–transfected ldlA7 cells. Therefore, rHDL-induced NO production, probably through an Akt/ERK/NO pathway in endothelial cells, may induce an antiarrhythmogenic effect. The HDL-based therapy may hold the promise of reducing the incidence of such arrhythmias after ischemia/reperfusion.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2007.12.040</identifier><identifier>PMID: 18420105</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Anti-Arrhythmia Agents - pharmacology ; Anti-Arrhythmia Agents - therapeutic use ; Apolipoprotein A-I - blood ; Apolipoprotein A-I - therapeutic use ; Biological and medical sciences ; Blood pressure ; Cardiology ; Cardiology. Vascular system ; Cardiovascular ; Cardiovascular disease ; Cholesterol ; Cholesterol, HDL - blood ; Cholesterol, HDL - pharmacology ; Cholesterol, HDL - therapeutic use ; Endothelium ; Extracellular Signal-Regulated MAP Kinases - drug effects ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Heart ; Heart attacks ; Heart rate ; Internal Medicine ; Ischemia ; Lipoproteins ; Male ; Medical sciences ; Myocardial Ischemia - physiopathology ; Myocardial Ischemia - prevention & control ; Myocardial Reperfusion - adverse effects ; Nitric Oxide - metabolism ; Ostomy ; Proto-Oncogene Proteins c-akt - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Wistar ; Rodents ; Signal Transduction ; Studies ; Tachycardia, Ventricular - etiology ; Tachycardia, Ventricular - physiopathology ; Tachycardia, Ventricular - prevention & control</subject><ispartof>Journal of the American College of Cardiology, 2008-04, Vol.51 (16), p.1604-1612</ispartof><rights>American College of Cardiology Foundation</rights><rights>2008 American College of Cardiology Foundation</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Elsevier Limited Apr 22, 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-526ebe67ff21ca1d82e3b521e71b74e5154cd9d4e1da363f4c7acf890881ce3c3</citedby><cites>FETCH-LOGICAL-c569t-526ebe67ff21ca1d82e3b521e71b74e5154cd9d4e1da363f4c7acf890881ce3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735109708004105$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20267395$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18420105$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Imaizumi, Satoshi, MD</creatorcontrib><creatorcontrib>Miura, Shin-ichiro, MD, PhD</creatorcontrib><creatorcontrib>Nakamura, Kazuto, MD, PhD</creatorcontrib><creatorcontrib>Kiya, Yoshihiro, MD</creatorcontrib><creatorcontrib>Uehara, Yoshinari, MD, PhD</creatorcontrib><creatorcontrib>Zhang, Bo, PhD</creatorcontrib><creatorcontrib>Matsuo, Yoshino, PhD</creatorcontrib><creatorcontrib>Urata, Hidenori, MD, PhD</creatorcontrib><creatorcontrib>Ideishi, Munehito, MD, PhD</creatorcontrib><creatorcontrib>Rye, Kerry-Anne, PhD</creatorcontrib><creatorcontrib>Sata, Masataka, MD, PhD</creatorcontrib><creatorcontrib>Saku, Keijiro, MD, PhD, FACC</creatorcontrib><title>Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats Satoshi Imaizumi, Shin-ichiro Miura, Kazuto Nakamura, Yoshihiro Kiya, Yoshinari Uehara, Bo Zhang, Yoshino Matsuo, Hidenori Urata, Munehito Ideishi, Kerry-Anne Rye, Masataka Sata, Keijiro Saku We analyzed the suppression of reperfusion-induced arrhythmias by reconstituted high-density lipoprotein (rHDL) in rats. Ventricular arrhythmias after reperfusion in rHDL–pre-treated rats were significantly suppressed. This effect was mediated by an Akt protein kinase/extracellular-signal-regulated kinase (ERK)/endothelial nitric oxide (NO) synthesis pathway. We also found that rHDL activated Akt/ERK/NO in human coronary artery endothelial cells. In addition, rHDL activated ERK in adenosine triphosphate-binding cassette transporter A1- or G1-transfected but not scavenger receptor class B, type I–transfected ldlA7 cells. Therefore, rHDL-induced NO production, probably through an Akt/ERK/NO pathway in endothelial cells, may induce an antiarrhythmogenic effect. The HDL-based therapy may hold the promise of reducing the incidence of such arrhythmias after ischemia/reperfusion.</description><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Anti-Arrhythmia Agents - therapeutic use</subject><subject>Apolipoprotein A-I - blood</subject><subject>Apolipoprotein A-I - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blood pressure</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Cardiovascular disease</subject><subject>Cholesterol</subject><subject>Cholesterol, HDL - blood</subject><subject>Cholesterol, HDL - pharmacology</subject><subject>Cholesterol, HDL - therapeutic use</subject><subject>Endothelium</subject><subject>Extracellular Signal-Regulated MAP Kinases - drug effects</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Heart</subject><subject>Heart attacks</subject><subject>Heart rate</subject><subject>Internal Medicine</subject><subject>Ischemia</subject><subject>Lipoproteins</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Ischemia - prevention & control</subject><subject>Myocardial Reperfusion - adverse effects</subject><subject>Nitric Oxide - metabolism</subject><subject>Ostomy</subject><subject>Proto-Oncogene Proteins c-akt - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Studies</subject><subject>Tachycardia, Ventricular - etiology</subject><subject>Tachycardia, Ventricular - physiopathology</subject><subject>Tachycardia, Ventricular - prevention & control</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kl2L1DAUhoso7uzqH_BCCuLetXtO2vQDRBjW1V0YEEa9Dpn0ZJrajzFJhfn3ps7gwl54lYs87-HNeRJFbxBSBCxuurSTSqUMoEyRpZDDs2iFnFdJxuvyebSCMuMJQl1eRJfOdQBQVFi_jC6wyhkg8FXUrkdvpLXt0bfDtKfRqPhOa1I-nnS8JTWNzhs_e2rie7Nvk080OuOP8cYcpoOdPJkxXu-lCVj84FRLg5E3WzqQ1bMz0xiH-6307lX0Qsve0evzeRX9-Hz3_fY-2Xz98nC73iSKF7VPOCtoR0WpNUMlsakYZTvOkErclTlx5Llq6iYnbGRWZDpXpVS6qqGqUFGmsqvo-jQ3lPs1k_NiME5R38uRptmJokbMypoH8N0TsJtmO4ZuAjkUDGrAhWInStnJOUtaHKwZpD0KBLFYEJ1YLIjFgkAmgoUQensePe8Gah4j57UH4P0ZkE7JXls5KuP-cQxYUWZ_O344cRQ29tuQFU4ZGhU1xgZFopnM_3t8fBJXvQmGZf-TjuQe3ytcCIhvy39ZvgtUAPnS8w-PGLsB</recordid><startdate>20080422</startdate><enddate>20080422</enddate><creator>Imaizumi, Satoshi, MD</creator><creator>Miura, Shin-ichiro, MD, PhD</creator><creator>Nakamura, Kazuto, MD, PhD</creator><creator>Kiya, Yoshihiro, MD</creator><creator>Uehara, Yoshinari, MD, PhD</creator><creator>Zhang, Bo, PhD</creator><creator>Matsuo, Yoshino, PhD</creator><creator>Urata, Hidenori, MD, PhD</creator><creator>Ideishi, Munehito, MD, PhD</creator><creator>Rye, Kerry-Anne, PhD</creator><creator>Sata, Masataka, MD, PhD</creator><creator>Saku, Keijiro, MD, PhD, FACC</creator><general>Elsevier Inc</general><general>Elsevier Science</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20080422</creationdate><title>Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats</title><author>Imaizumi, Satoshi, MD ; Miura, Shin-ichiro, MD, PhD ; Nakamura, Kazuto, MD, PhD ; Kiya, Yoshihiro, MD ; Uehara, Yoshinari, MD, PhD ; Zhang, Bo, PhD ; Matsuo, Yoshino, PhD ; Urata, Hidenori, MD, PhD ; Ideishi, Munehito, MD, PhD ; Rye, Kerry-Anne, PhD ; Sata, Masataka, MD, PhD ; Saku, Keijiro, MD, PhD, FACC</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-526ebe67ff21ca1d82e3b521e71b74e5154cd9d4e1da363f4c7acf890881ce3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Anti-Arrhythmia Agents - therapeutic use</topic><topic>Apolipoprotein A-I - blood</topic><topic>Apolipoprotein A-I - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blood pressure</topic><topic>Cardiology</topic><topic>Cardiology. 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Ventricular arrhythmias after reperfusion in rHDL–pre-treated rats were significantly suppressed. This effect was mediated by an Akt protein kinase/extracellular-signal-regulated kinase (ERK)/endothelial nitric oxide (NO) synthesis pathway. We also found that rHDL activated Akt/ERK/NO in human coronary artery endothelial cells. In addition, rHDL activated ERK in adenosine triphosphate-binding cassette transporter A1- or G1-transfected but not scavenger receptor class B, type I–transfected ldlA7 cells. Therefore, rHDL-induced NO production, probably through an Akt/ERK/NO pathway in endothelial cells, may induce an antiarrhythmogenic effect. The HDL-based therapy may hold the promise of reducing the incidence of such arrhythmias after ischemia/reperfusion.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>18420105</pmid><doi>10.1016/j.jacc.2007.12.040</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Anti-Arrhythmia Agents - pharmacology Anti-Arrhythmia Agents - therapeutic use Apolipoprotein A-I - blood Apolipoprotein A-I - therapeutic use Biological and medical sciences Blood pressure Cardiology Cardiology. Vascular system Cardiovascular Cardiovascular disease Cholesterol Cholesterol, HDL - blood Cholesterol, HDL - pharmacology Cholesterol, HDL - therapeutic use Endothelium Extracellular Signal-Regulated MAP Kinases - drug effects Extracellular Signal-Regulated MAP Kinases - metabolism Heart Heart attacks Heart rate Internal Medicine Ischemia Lipoproteins Male Medical sciences Myocardial Ischemia - physiopathology Myocardial Ischemia - prevention & control Myocardial Reperfusion - adverse effects Nitric Oxide - metabolism Ostomy Proto-Oncogene Proteins c-akt - drug effects Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar Rodents Signal Transduction Studies Tachycardia, Ventricular - etiology Tachycardia, Ventricular - physiopathology Tachycardia, Ventricular - prevention & control |
title | Antiarrhythmogenic Effect of Reconstituted High-Density Lipoprotein Against Ischemia/Reperfusion in Rats |
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