Cyclic Adenosine Monophosphate Inhibits Quinolone Alkaloid Evocarpine‐Induced Apoptosis via Activation of Protein Kinase A in Human Leukaemic HL‐60 Cells

: Evocarpine, an isoquinolone alkaloid isolated from the fruit of Evodia rutaecarpa, was found to induce apoptotic cell death in promyelocytic leukaemia HL‐60 cells in dose‐ and time‐dependent manners. We investigated the involvement of protein kinase A during the evocarpine‐induced apoptotic cell d...

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Veröffentlicht in:Pharmacology & toxicology 2000-07, Vol.87 (1), p.1-5
Hauptverfasser: Kim, Na‐Young, Pae, Hyun‐Ock, Kang, Tai‐Hyun, Kim, Youn‐Chul, Lee, Ho‐Sub, Chung, Hun‐Taeg
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container_title Pharmacology & toxicology
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creator Kim, Na‐Young
Pae, Hyun‐Ock
Kang, Tai‐Hyun
Kim, Youn‐Chul
Lee, Ho‐Sub
Chung, Hun‐Taeg
description : Evocarpine, an isoquinolone alkaloid isolated from the fruit of Evodia rutaecarpa, was found to induce apoptotic cell death in promyelocytic leukaemia HL‐60 cells in dose‐ and time‐dependent manners. We investigated the involvement of protein kinase A during the evocarpine‐induced apoptotic cell death. Evocarpine‐induced apoptosis was markedly inhibited by treatment of the cells with dibutyryl‐cyclic adenosine monophosphate. Similar results were obtained with other commonly used cyclic adenosine monophosphate analogues, chlorophenylthio‐cyclic adenosine monophosphate and the intracellular cyclic adenosine monophosphate‐elevating agent, forskolin. In contrast, pretreatment of HL‐60 cells with KT5720, an inhibitor of cyclic adenosine monophosphate‐dependent protein kinase A, abrogated the protective effects of cyclic adenosine monophosphate analogues and forskolin on evocrpine‐induced apoptosis. These findings suggest that cyclic adenosine monophosphate‐dependent activation of protein kinase A plays a crucial role in protecting HL‐60 cells from the evocarpine‐induced apoptotic cell death.
doi_str_mv 10.1111/j.0901-9928.2000.870101.x
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We investigated the involvement of protein kinase A during the evocarpine‐induced apoptotic cell death. Evocarpine‐induced apoptosis was markedly inhibited by treatment of the cells with dibutyryl‐cyclic adenosine monophosphate. Similar results were obtained with other commonly used cyclic adenosine monophosphate analogues, chlorophenylthio‐cyclic adenosine monophosphate and the intracellular cyclic adenosine monophosphate‐elevating agent, forskolin. In contrast, pretreatment of HL‐60 cells with KT5720, an inhibitor of cyclic adenosine monophosphate‐dependent protein kinase A, abrogated the protective effects of cyclic adenosine monophosphate analogues and forskolin on evocrpine‐induced apoptosis. These findings suggest that cyclic adenosine monophosphate‐dependent activation of protein kinase A plays a crucial role in protecting HL‐60 cells from the evocarpine‐induced apoptotic cell death.</description><identifier>ISSN: 0901-9928</identifier><identifier>EISSN: 1600-0773</identifier><identifier>DOI: 10.1111/j.0901-9928.2000.870101.x</identifier><identifier>PMID: 10987208</identifier><identifier>CODEN: PHTOEH</identifier><language>eng</language><publisher>Copenhagen: Munksgaard International Publishers</publisher><subject>Ageing, cell death ; Apoptosis - drug effects ; Biological and medical sciences ; Cell physiology ; Cyclic AMP - analogs &amp; derivatives ; Cyclic AMP - pharmacology ; Cyclic AMP-Dependent Protein Kinases - drug effects ; DNA Fragmentation - drug effects ; Electrophoresis, Agar Gel ; Fundamental and applied biological sciences. 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We investigated the involvement of protein kinase A during the evocarpine‐induced apoptotic cell death. Evocarpine‐induced apoptosis was markedly inhibited by treatment of the cells with dibutyryl‐cyclic adenosine monophosphate. Similar results were obtained with other commonly used cyclic adenosine monophosphate analogues, chlorophenylthio‐cyclic adenosine monophosphate and the intracellular cyclic adenosine monophosphate‐elevating agent, forskolin. In contrast, pretreatment of HL‐60 cells with KT5720, an inhibitor of cyclic adenosine monophosphate‐dependent protein kinase A, abrogated the protective effects of cyclic adenosine monophosphate analogues and forskolin on evocrpine‐induced apoptosis. These findings suggest that cyclic adenosine monophosphate‐dependent activation of protein kinase A plays a crucial role in protecting HL‐60 cells from the evocarpine‐induced apoptotic cell death.</description><subject>Ageing, cell death</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cyclic AMP - analogs &amp; derivatives</subject><subject>Cyclic AMP - pharmacology</subject><subject>Cyclic AMP-Dependent Protein Kinases - drug effects</subject><subject>DNA Fragmentation - drug effects</subject><subject>Electrophoresis, Agar Gel</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>Molecular and cellular biology</subject><subject>Quinolones - antagonists &amp; inhibitors</subject><issn>0901-9928</issn><issn>1600-0773</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU9u1DAYxSMEoqPSKyAjIXYJn504dpYhKsyIQRSprC3HcTRuEzvEybSz4whcgMtxEhxlBCzxxn_0e89P34uiVxgSHNbbuwQKwHFREJ4QAEg4Aww4eXwSbXAOEANj6dNo84e6iK68NzWklHGMs_x5dIGh4IwA30Q_q5PqjEJlo63zxmr0yVk3HJwfDnLSaGcPpjaTR19mY13nAlB297JzpkHXR6fkOATRr-8_draZlW5QObhhCk4eHY1EpZrMUU7GWeRadDO6SRuLPhorfTBC4byde2nRXs_3UvchyHYfzHJAle46_yJ61srO66vzfhl9fX99W23j_ecPu6rcx4pihmOaa4ppWzNKKWOsVhhoW6Q5C0-kBg40awpJ8oa3pFYsJzJtWE4zjpuU4Zanl9Gb1XcY3bdZ-0n0xquQQFrtZi8YIZQTTgJYrKAanfejbsUwml6OJ4FBLPWIO7EMXiyDF0s9Yq1HPAbty_Mnc93r5h_lWkYAXp8B6ZXs2lFaZfxfLstyIEuGcsUeTKdP_x9AvKtubtdL-hvp8K5H</recordid><startdate>200007</startdate><enddate>200007</enddate><creator>Kim, Na‐Young</creator><creator>Pae, Hyun‐Ock</creator><creator>Kang, Tai‐Hyun</creator><creator>Kim, Youn‐Chul</creator><creator>Lee, Ho‐Sub</creator><creator>Chung, Hun‐Taeg</creator><general>Munksgaard International Publishers</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>7X8</scope></search><sort><creationdate>200007</creationdate><title>Cyclic Adenosine Monophosphate Inhibits Quinolone Alkaloid Evocarpine‐Induced Apoptosis via Activation of Protein Kinase A in Human Leukaemic HL‐60 Cells</title><author>Kim, Na‐Young ; Pae, Hyun‐Ock ; Kang, Tai‐Hyun ; Kim, Youn‐Chul ; Lee, Ho‐Sub ; Chung, Hun‐Taeg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5171-56e515fb7555777bc105f9367fb72b08054d9a26d8f2bc762a3d765481d371f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Ageing, cell death</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cyclic AMP - analogs &amp; derivatives</topic><topic>Cyclic AMP - pharmacology</topic><topic>Cyclic AMP-Dependent Protein Kinases - drug effects</topic><topic>DNA Fragmentation - drug effects</topic><topic>Electrophoresis, Agar Gel</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Molecular and cellular biology</topic><topic>Quinolones - antagonists &amp; inhibitors</topic><toplevel>online_resources</toplevel><creatorcontrib>Kim, Na‐Young</creatorcontrib><creatorcontrib>Pae, Hyun‐Ock</creatorcontrib><creatorcontrib>Kang, Tai‐Hyun</creatorcontrib><creatorcontrib>Kim, Youn‐Chul</creatorcontrib><creatorcontrib>Lee, Ho‐Sub</creatorcontrib><creatorcontrib>Chung, Hun‐Taeg</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>Pharmacology &amp; toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Na‐Young</au><au>Pae, Hyun‐Ock</au><au>Kang, Tai‐Hyun</au><au>Kim, Youn‐Chul</au><au>Lee, Ho‐Sub</au><au>Chung, Hun‐Taeg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclic Adenosine Monophosphate Inhibits Quinolone Alkaloid Evocarpine‐Induced Apoptosis via Activation of Protein Kinase A in Human Leukaemic HL‐60 Cells</atitle><jtitle>Pharmacology &amp; toxicology</jtitle><addtitle>Pharmacol Toxicol</addtitle><date>2000-07</date><risdate>2000</risdate><volume>87</volume><issue>1</issue><spage>1</spage><epage>5</epage><pages>1-5</pages><issn>0901-9928</issn><eissn>1600-0773</eissn><coden>PHTOEH</coden><abstract>: Evocarpine, an isoquinolone alkaloid isolated from the fruit of Evodia rutaecarpa, was found to induce apoptotic cell death in promyelocytic leukaemia HL‐60 cells in dose‐ and time‐dependent manners. 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source MEDLINE; Wiley Online Library Journals Frontfile Complete; Alma/SFX Local Collection
subjects Ageing, cell death
Apoptosis - drug effects
Biological and medical sciences
Cell physiology
Cyclic AMP - analogs & derivatives
Cyclic AMP - pharmacology
Cyclic AMP-Dependent Protein Kinases - drug effects
DNA Fragmentation - drug effects
Electrophoresis, Agar Gel
Fundamental and applied biological sciences. Psychology
HL-60 Cells
Humans
Molecular and cellular biology
Quinolones - antagonists & inhibitors
title Cyclic Adenosine Monophosphate Inhibits Quinolone Alkaloid Evocarpine‐Induced Apoptosis via Activation of Protein Kinase A in Human Leukaemic HL‐60 Cells
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