Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion
: Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardi...
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| creator | Li, Hong‐zhu Han, Li‐ping Jiang, Chun‐ming Li, Hong Zhao, Ya‐jun Gao, Jun Lin, Yan Ma, Shu‐xia Tian, Ye Yang, Bao‐feng Xu, Chang‐qing |
| description | : Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardiomyocytes in ischaemia‐mimetic solution for 2 hr, followed by incubation in normal culture medium for 24 hr. Lactate dehydrogenase activity, superoxide dismutase activity and malondialdehyde content were determined colorimetrically with a spectrophotometer. Apoptotic cell death was assayed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick end labelling staining and flow cytometry, and morphological alterations were observed with transmission electron microscopy. The intracellular free calcium concentration ([Ca2+]i) was measured by confocal laser scanning microscopy. Finally, the expression of dopamine receptor 1 (DR1), caspase‐3, ‐8 and ‐9, Fas, Fas ligand and Bcl‐2 and the release of cytochrome c were analysed by Western blot. The results showed that DR1 expression was increased markedly during ischaemia/reperfusion. Treatment with 10 µM SKF‐38393 (DR1 agonist) significantly increased lactate dehydrogenase activity, decreased superoxide dismutase activity and increased malondialdehyde content in the culture medium. The DR1 agonist promoted the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischaemia/reperfusion. Furthermore, SKF‐38393 up‐regulated the expression of caspase‐3, ‐8 and ‐9, Fas and Fas ligand, and down‐regulated Bcl‐2 expression. In contrast, 10 µM SCH‐23390 (DR1 antagonist) had no significant effects on the above indicators. In conclusion, DR1 activation is involved in the apoptosis of cultured neonatal rat cardiomyocytes in simulated ischaemia/reperfusion through the mitochondrial and death receptor pathways. |
| doi_str_mv | 10.1111/j.1742-7843.2007.00177.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70326829</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20465303</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5447-612b49842bf581f03f62887d8daf53a86ddde9265c98cb86899d66bf0cbc91713</originalsourceid><addsrcrecordid>eNqNkUtv1DAQgC0EoqXwF5AvcNvUr9jOgUMJpa1UAVrK2XL8EF4lcbATtfvvcdjVcoS5zFj-ZmzNBwDEqMIlLncVFoxshGS0IgiJCiEsRPX0DJyfLp6falqfgVc57xAigmH0EpxhSRqGBT8Hy7X3zswwevgpTnoIo4NbZ9w0xwQxjCO8mmI55JBXpl36eUnOwi8ujnrWPdzqGbY62RCHfTT72WUYRvg9DEuv5wLeZfNTuyHoy62bXPJLDnF8DV543Wf35pgvwI_P1w_t7eb-681de3W_MTVjYsMx6VgjGel8LbFH1HMipbDSal9TLbm11jWE16aRppNcNo3lvPPIdKbBAtML8P4wd0rx1-LyrIaQjet7Pbq4ZCUQJbzs4p8gQYzXFNECygNoUsw5Oa-mFAad9gojtbpRO7WuXa0K1OpG_XGjnkrr2-MbSzc4-7fxKKMA746Azkb3PunRhHziCMKEcIIK9-HAPYbe7f_7A-pj--2hVPQ3kmmqrQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20465303</pqid></control><display><type>article</type><title>Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><source>Alma/SFX Local Collection</source><creator>Li, Hong‐zhu ; Han, Li‐ping ; Jiang, Chun‐ming ; Li, Hong ; Zhao, Ya‐jun ; Gao, Jun ; Lin, Yan ; Ma, Shu‐xia ; Tian, Ye ; Yang, Bao‐feng ; Xu, Chang‐qing</creator><creatorcontrib>Li, Hong‐zhu ; Han, Li‐ping ; Jiang, Chun‐ming ; Li, Hong ; Zhao, Ya‐jun ; Gao, Jun ; Lin, Yan ; Ma, Shu‐xia ; Tian, Ye ; Yang, Bao‐feng ; Xu, Chang‐qing</creatorcontrib><description>: Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardiomyocytes in ischaemia‐mimetic solution for 2 hr, followed by incubation in normal culture medium for 24 hr. Lactate dehydrogenase activity, superoxide dismutase activity and malondialdehyde content were determined colorimetrically with a spectrophotometer. Apoptotic cell death was assayed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick end labelling staining and flow cytometry, and morphological alterations were observed with transmission electron microscopy. The intracellular free calcium concentration ([Ca2+]i) was measured by confocal laser scanning microscopy. Finally, the expression of dopamine receptor 1 (DR1), caspase‐3, ‐8 and ‐9, Fas, Fas ligand and Bcl‐2 and the release of cytochrome c were analysed by Western blot. The results showed that DR1 expression was increased markedly during ischaemia/reperfusion. Treatment with 10 µM SKF‐38393 (DR1 agonist) significantly increased lactate dehydrogenase activity, decreased superoxide dismutase activity and increased malondialdehyde content in the culture medium. The DR1 agonist promoted the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischaemia/reperfusion. Furthermore, SKF‐38393 up‐regulated the expression of caspase‐3, ‐8 and ‐9, Fas and Fas ligand, and down‐regulated Bcl‐2 expression. In contrast, 10 µM SCH‐23390 (DR1 antagonist) had no significant effects on the above indicators. In conclusion, DR1 activation is involved in the apoptosis of cultured neonatal rat cardiomyocytes in simulated ischaemia/reperfusion through the mitochondrial and death receptor pathways.</description><identifier>ISSN: 1742-7835</identifier><identifier>EISSN: 1742-7843</identifier><identifier>DOI: 10.1111/j.1742-7843.2007.00177.x</identifier><identifier>PMID: 18294176</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Animals ; Animals, Newborn ; Apoptosis - physiology ; Biological and medical sciences ; Blotting, Western ; Calcium - metabolism ; Cardiology. Vascular system ; Caspases - metabolism ; Cells, Cultured ; Cytochromes c - metabolism ; Disease Models, Animal ; L-Lactate Dehydrogenase - metabolism ; Malondialdehyde - metabolism ; Medical sciences ; Mitochondria, Heart - metabolism ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocytes, Cardiac - metabolism ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; Receptors, Death Domain - metabolism ; Receptors, Dopamine D1 - genetics ; Receptors, Dopamine D1 - metabolism ; Superoxide Dismutase - metabolism</subject><ispartof>Basic & clinical pharmacology & toxicology, 2008-03, Vol.102 (3), p.329-336</ispartof><rights>2008 The Authors</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5447-612b49842bf581f03f62887d8daf53a86ddde9265c98cb86899d66bf0cbc91713</citedby><cites>FETCH-LOGICAL-c5447-612b49842bf581f03f62887d8daf53a86ddde9265c98cb86899d66bf0cbc91713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1742-7843.2007.00177.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1742-7843.2007.00177.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20122620$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18294176$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Hong‐zhu</creatorcontrib><creatorcontrib>Han, Li‐ping</creatorcontrib><creatorcontrib>Jiang, Chun‐ming</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><creatorcontrib>Zhao, Ya‐jun</creatorcontrib><creatorcontrib>Gao, Jun</creatorcontrib><creatorcontrib>Lin, Yan</creatorcontrib><creatorcontrib>Ma, Shu‐xia</creatorcontrib><creatorcontrib>Tian, Ye</creatorcontrib><creatorcontrib>Yang, Bao‐feng</creatorcontrib><creatorcontrib>Xu, Chang‐qing</creatorcontrib><title>Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion</title><title>Basic & clinical pharmacology & toxicology</title><addtitle>Basic Clin Pharmacol Toxicol</addtitle><description>: Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardiomyocytes in ischaemia‐mimetic solution for 2 hr, followed by incubation in normal culture medium for 24 hr. Lactate dehydrogenase activity, superoxide dismutase activity and malondialdehyde content were determined colorimetrically with a spectrophotometer. Apoptotic cell death was assayed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick end labelling staining and flow cytometry, and morphological alterations were observed with transmission electron microscopy. The intracellular free calcium concentration ([Ca2+]i) was measured by confocal laser scanning microscopy. Finally, the expression of dopamine receptor 1 (DR1), caspase‐3, ‐8 and ‐9, Fas, Fas ligand and Bcl‐2 and the release of cytochrome c were analysed by Western blot. The results showed that DR1 expression was increased markedly during ischaemia/reperfusion. Treatment with 10 µM SKF‐38393 (DR1 agonist) significantly increased lactate dehydrogenase activity, decreased superoxide dismutase activity and increased malondialdehyde content in the culture medium. The DR1 agonist promoted the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischaemia/reperfusion. Furthermore, SKF‐38393 up‐regulated the expression of caspase‐3, ‐8 and ‐9, Fas and Fas ligand, and down‐regulated Bcl‐2 expression. In contrast, 10 µM SCH‐23390 (DR1 antagonist) had no significant effects on the above indicators. In conclusion, DR1 activation is involved in the apoptosis of cultured neonatal rat cardiomyocytes in simulated ischaemia/reperfusion through the mitochondrial and death receptor pathways.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Calcium - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Caspases - metabolism</subject><subject>Cells, Cultured</subject><subject>Cytochromes c - metabolism</subject><subject>Disease Models, Animal</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Malondialdehyde - metabolism</subject><subject>Medical sciences</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Death Domain - metabolism</subject><subject>Receptors, Dopamine D1 - genetics</subject><subject>Receptors, Dopamine D1 - metabolism</subject><subject>Superoxide Dismutase - metabolism</subject><issn>1742-7835</issn><issn>1742-7843</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtv1DAQgC0EoqXwF5AvcNvUr9jOgUMJpa1UAVrK2XL8EF4lcbATtfvvcdjVcoS5zFj-ZmzNBwDEqMIlLncVFoxshGS0IgiJCiEsRPX0DJyfLp6falqfgVc57xAigmH0EpxhSRqGBT8Hy7X3zswwevgpTnoIo4NbZ9w0xwQxjCO8mmI55JBXpl36eUnOwi8ujnrWPdzqGbY62RCHfTT72WUYRvg9DEuv5wLeZfNTuyHoy62bXPJLDnF8DV543Wf35pgvwI_P1w_t7eb-681de3W_MTVjYsMx6VgjGel8LbFH1HMipbDSal9TLbm11jWE16aRppNcNo3lvPPIdKbBAtML8P4wd0rx1-LyrIaQjet7Pbq4ZCUQJbzs4p8gQYzXFNECygNoUsw5Oa-mFAad9gojtbpRO7WuXa0K1OpG_XGjnkrr2-MbSzc4-7fxKKMA746Azkb3PunRhHziCMKEcIIK9-HAPYbe7f_7A-pj--2hVPQ3kmmqrQ</recordid><startdate>200803</startdate><enddate>200803</enddate><creator>Li, Hong‐zhu</creator><creator>Han, Li‐ping</creator><creator>Jiang, Chun‐ming</creator><creator>Li, Hong</creator><creator>Zhao, Ya‐jun</creator><creator>Gao, Jun</creator><creator>Lin, Yan</creator><creator>Ma, Shu‐xia</creator><creator>Tian, Ye</creator><creator>Yang, Bao‐feng</creator><creator>Xu, Chang‐qing</creator><general>Blackwell Publishing Inc</general><general>Blackwell</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>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>200803</creationdate><title>Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion</title><author>Li, Hong‐zhu ; Han, Li‐ping ; Jiang, Chun‐ming ; Li, Hong ; Zhao, Ya‐jun ; Gao, Jun ; Lin, Yan ; Ma, Shu‐xia ; Tian, Ye ; Yang, Bao‐feng ; Xu, Chang‐qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5447-612b49842bf581f03f62887d8daf53a86ddde9265c98cb86899d66bf0cbc91713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Calcium - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Caspases - metabolism</topic><topic>Cells, Cultured</topic><topic>Cytochromes c - metabolism</topic><topic>Disease Models, Animal</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Malondialdehyde - metabolism</topic><topic>Medical sciences</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Death Domain - metabolism</topic><topic>Receptors, Dopamine D1 - genetics</topic><topic>Receptors, Dopamine D1 - metabolism</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Hong‐zhu</creatorcontrib><creatorcontrib>Han, Li‐ping</creatorcontrib><creatorcontrib>Jiang, Chun‐ming</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><creatorcontrib>Zhao, Ya‐jun</creatorcontrib><creatorcontrib>Gao, Jun</creatorcontrib><creatorcontrib>Lin, Yan</creatorcontrib><creatorcontrib>Ma, Shu‐xia</creatorcontrib><creatorcontrib>Tian, Ye</creatorcontrib><creatorcontrib>Yang, Bao‐feng</creatorcontrib><creatorcontrib>Xu, Chang‐qing</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Basic & clinical pharmacology & toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Hong‐zhu</au><au>Han, Li‐ping</au><au>Jiang, Chun‐ming</au><au>Li, Hong</au><au>Zhao, Ya‐jun</au><au>Gao, Jun</au><au>Lin, Yan</au><au>Ma, Shu‐xia</au><au>Tian, Ye</au><au>Yang, Bao‐feng</au><au>Xu, Chang‐qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion</atitle><jtitle>Basic & clinical pharmacology & toxicology</jtitle><addtitle>Basic Clin Pharmacol Toxicol</addtitle><date>2008-03</date><risdate>2008</risdate><volume>102</volume><issue>3</issue><spage>329</spage><epage>336</epage><pages>329-336</pages><issn>1742-7835</issn><eissn>1742-7843</eissn><abstract>: Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardiomyocytes in ischaemia‐mimetic solution for 2 hr, followed by incubation in normal culture medium for 24 hr. Lactate dehydrogenase activity, superoxide dismutase activity and malondialdehyde content were determined colorimetrically with a spectrophotometer. Apoptotic cell death was assayed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick end labelling staining and flow cytometry, and morphological alterations were observed with transmission electron microscopy. The intracellular free calcium concentration ([Ca2+]i) was measured by confocal laser scanning microscopy. Finally, the expression of dopamine receptor 1 (DR1), caspase‐3, ‐8 and ‐9, Fas, Fas ligand and Bcl‐2 and the release of cytochrome c were analysed by Western blot. The results showed that DR1 expression was increased markedly during ischaemia/reperfusion. Treatment with 10 µM SKF‐38393 (DR1 agonist) significantly increased lactate dehydrogenase activity, decreased superoxide dismutase activity and increased malondialdehyde content in the culture medium. The DR1 agonist promoted the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischaemia/reperfusion. Furthermore, SKF‐38393 up‐regulated the expression of caspase‐3, ‐8 and ‐9, Fas and Fas ligand, and down‐regulated Bcl‐2 expression. In contrast, 10 µM SCH‐23390 (DR1 antagonist) had no significant effects on the above indicators. In conclusion, DR1 activation is involved in the apoptosis of cultured neonatal rat cardiomyocytes in simulated ischaemia/reperfusion through the mitochondrial and death receptor pathways.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>18294176</pmid><doi>10.1111/j.1742-7843.2007.00177.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Newborn Apoptosis - physiology Biological and medical sciences Blotting, Western Calcium - metabolism Cardiology. Vascular system Caspases - metabolism Cells, Cultured Cytochromes c - metabolism Disease Models, Animal L-Lactate Dehydrogenase - metabolism Malondialdehyde - metabolism Medical sciences Mitochondria, Heart - metabolism Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocytes, Cardiac - metabolism Pharmacology. Drug treatments Rats Rats, Wistar Receptors, Death Domain - metabolism Receptors, Dopamine D1 - genetics Receptors, Dopamine D1 - metabolism Superoxide Dismutase - metabolism |
| title | Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion |
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