Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death
Caffeine is a globally consumed psychostimulant but can be fatal to cells at overdose exposures. Although caspase-dependent apoptosis plays a role in caffeine-induced cell death, the responsible intracellular signalling cascade remains incompletely understood. The cellular slime mould, Dictyostelium...
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| description | Caffeine is a globally consumed psychostimulant but can be fatal to cells at overdose exposures. Although caspase-dependent apoptosis plays a role in caffeine-induced cell death, the responsible intracellular signalling cascade remains incompletely understood. The cellular slime mould,
Dictyostelium discoideum
, does not possess caspase-dependent apoptotic machinery. Here, we observed that ablation of
D. discoideum
plaA,
which encodes a phospholipase A2 (PLA
2
) homolog, leads to a decreased rate of cell death under high caffeine concentrations and to enhanced cell death with the addition of arachidonic acid. Moreover, the inhibition of PLA
2
activity lead to a recovery of the survival rate in caspase-inhibited Hela cervical carcinoma cells under high caffeine concentrations, indicating that caffeine-induced cell death is enhanced via PLA
2
-dependent signalling. Our results indicate that arachidonic acid may be a general second messenger that negatively regulates caffeine tolerance via a caspase-independent cell death cascade, which leads to multiple effects in eukaryotic cells. |
| doi_str_mv | 10.1038/srep00577 |
| format | Article |
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Dictyostelium discoideum
, does not possess caspase-dependent apoptotic machinery. Here, we observed that ablation of
D. discoideum
plaA,
which encodes a phospholipase A2 (PLA
2
) homolog, leads to a decreased rate of cell death under high caffeine concentrations and to enhanced cell death with the addition of arachidonic acid. Moreover, the inhibition of PLA
2
activity lead to a recovery of the survival rate in caspase-inhibited Hela cervical carcinoma cells under high caffeine concentrations, indicating that caffeine-induced cell death is enhanced via PLA
2
-dependent signalling. Our results indicate that arachidonic acid may be a general second messenger that negatively regulates caffeine tolerance via a caspase-independent cell death cascade, which leads to multiple effects in eukaryotic cells.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep00577</identifier><identifier>PMID: 22896810</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/154/570 ; 631/208/325 ; 631/326/88 ; 631/80/82 ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Arachidonic acid ; Arachidonic Acid - pharmacology ; Caffeine ; Caffeine - pharmacology ; Caspase ; Caspases - metabolism ; Cell death ; Cell Survival - drug effects ; Cervical cancer ; Cervical carcinoma ; Cervix ; Cyclic AMP - metabolism ; Dictyostelium - drug effects ; Dictyostelium - genetics ; Dictyostelium - metabolism ; Drug Resistance ; Drug Synergism ; Enzyme Activation - drug effects ; HeLa Cells ; Humanities and Social Sciences ; Humans ; Intracellular signalling ; Mortality ; multidisciplinary ; Overdose ; Phospholipase A2 ; Phospholipases A2 - metabolism ; Science ; Signal Transduction - drug effects ; Survival</subject><ispartof>Scientific reports, 2012-08, Vol.2 (1), p.577, Article 577</ispartof><rights>The Author(s) 2012</rights><rights>Copyright Nature Publishing Group Aug 2012</rights><rights>Copyright © 2012, Macmillan Publishers Limited. All rights reserved 2012 Macmillan Publishers Limited. All rights reserved</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c548t-9e480408cb74ca9d0262b7ea3c2b785ab847bacc6dee84c8fbcbeb1b395ea53b3</citedby><cites>FETCH-LOGICAL-c548t-9e480408cb74ca9d0262b7ea3c2b785ab847bacc6dee84c8fbcbeb1b395ea53b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419364/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419364/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27906,27907,41102,42171,51558,53773,53775</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22896810$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuwayama, Hidekazu</creatorcontrib><title>Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Caffeine is a globally consumed psychostimulant but can be fatal to cells at overdose exposures. Although caspase-dependent apoptosis plays a role in caffeine-induced cell death, the responsible intracellular signalling cascade remains incompletely understood. The cellular slime mould,
Dictyostelium discoideum
, does not possess caspase-dependent apoptotic machinery. Here, we observed that ablation of
D. discoideum
plaA,
which encodes a phospholipase A2 (PLA
2
) homolog, leads to a decreased rate of cell death under high caffeine concentrations and to enhanced cell death with the addition of arachidonic acid. Moreover, the inhibition of PLA
2
activity lead to a recovery of the survival rate in caspase-inhibited Hela cervical carcinoma cells under high caffeine concentrations, indicating that caffeine-induced cell death is enhanced via PLA
2
-dependent signalling. Our results indicate that arachidonic acid may be a general second messenger that negatively regulates caffeine tolerance via a caspase-independent cell death cascade, which leads to multiple effects in eukaryotic cells.</description><subject>631/154/570</subject><subject>631/208/325</subject><subject>631/326/88</subject><subject>631/80/82</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Arachidonic acid</subject><subject>Arachidonic Acid - pharmacology</subject><subject>Caffeine</subject><subject>Caffeine - pharmacology</subject><subject>Caspase</subject><subject>Caspases - metabolism</subject><subject>Cell death</subject><subject>Cell Survival - drug effects</subject><subject>Cervical cancer</subject><subject>Cervical carcinoma</subject><subject>Cervix</subject><subject>Cyclic AMP - metabolism</subject><subject>Dictyostelium - drug effects</subject><subject>Dictyostelium - genetics</subject><subject>Dictyostelium - metabolism</subject><subject>Drug Resistance</subject><subject>Drug Synergism</subject><subject>Enzyme Activation - drug effects</subject><subject>HeLa Cells</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Intracellular signalling</subject><subject>Mortality</subject><subject>multidisciplinary</subject><subject>Overdose</subject><subject>Phospholipase A2</subject><subject>Phospholipases A2 - metabolism</subject><subject>Science</subject><subject>Signal Transduction - drug effects</subject><subject>Survival</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkV9LwzAUxYMobsw9-AWk4JNCNU3SNn0RRp1_YOCLgm8hSW_Xji6tyTrw2xvdHBXzkHvh_Dj3cC9C5xG-iTDlt85Ch3GcpkdoTDCLQ0IJOR70IzR1boX9i0nGouwUjQjhWcIjPEbvMyt1VRetqXUw03URzE0ljQYX5LIsoTYQPpui11AEOTRNcA9yUwXbWnrdddL9yNCB_8xmgJyhk1I2Dqb7OkFvD_PX_ClcvDw-57NFqGPGN2EGjGOGuVYp0zIrMEmISkFS7QuPpeIsVVLrpADgTPNSaQUqUjSLQcZU0Qm62_l2vVpDoX0KKxvR2Xot7adoZS3-KqauxLLdCupXQRPmDS73Brb96MFtxKrtrfGZRcSzlGYpo9RTVztK29b5lZeHCREW33cQhzt49mIY6UD-bt0D1zvAeckswQ5G_nP7Avz4ksQ</recordid><startdate>20120815</startdate><enddate>20120815</enddate><creator>Kuwayama, Hidekazu</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20120815</creationdate><title>Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death</title><author>Kuwayama, Hidekazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c548t-9e480408cb74ca9d0262b7ea3c2b785ab847bacc6dee84c8fbcbeb1b395ea53b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>631/154/570</topic><topic>631/208/325</topic><topic>631/326/88</topic><topic>631/80/82</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Arachidonic acid</topic><topic>Arachidonic Acid - pharmacology</topic><topic>Caffeine</topic><topic>Caffeine - pharmacology</topic><topic>Caspase</topic><topic>Caspases - metabolism</topic><topic>Cell death</topic><topic>Cell Survival - drug effects</topic><topic>Cervical cancer</topic><topic>Cervical carcinoma</topic><topic>Cervix</topic><topic>Cyclic AMP - metabolism</topic><topic>Dictyostelium - drug effects</topic><topic>Dictyostelium - genetics</topic><topic>Dictyostelium - metabolism</topic><topic>Drug Resistance</topic><topic>Drug Synergism</topic><topic>Enzyme Activation - drug effects</topic><topic>HeLa Cells</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Intracellular signalling</topic><topic>Mortality</topic><topic>multidisciplinary</topic><topic>Overdose</topic><topic>Phospholipase A2</topic><topic>Phospholipases A2 - metabolism</topic><topic>Science</topic><topic>Signal Transduction - drug effects</topic><topic>Survival</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuwayama, Hidekazu</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kuwayama, Hidekazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2012-08-15</date><risdate>2012</risdate><volume>2</volume><issue>1</issue><spage>577</spage><pages>577-</pages><artnum>577</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Caffeine is a globally consumed psychostimulant but can be fatal to cells at overdose exposures. Although caspase-dependent apoptosis plays a role in caffeine-induced cell death, the responsible intracellular signalling cascade remains incompletely understood. The cellular slime mould,
Dictyostelium discoideum
, does not possess caspase-dependent apoptotic machinery. Here, we observed that ablation of
D. discoideum
plaA,
which encodes a phospholipase A2 (PLA
2
) homolog, leads to a decreased rate of cell death under high caffeine concentrations and to enhanced cell death with the addition of arachidonic acid. Moreover, the inhibition of PLA
2
activity lead to a recovery of the survival rate in caspase-inhibited Hela cervical carcinoma cells under high caffeine concentrations, indicating that caffeine-induced cell death is enhanced via PLA
2
-dependent signalling. Our results indicate that arachidonic acid may be a general second messenger that negatively regulates caffeine tolerance via a caspase-independent cell death cascade, which leads to multiple effects in eukaryotic cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>22896810</pmid><doi>10.1038/srep00577</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 631/154/570 631/208/325 631/326/88 631/80/82 Apoptosis Apoptosis - drug effects Apoptosis - genetics Arachidonic acid Arachidonic Acid - pharmacology Caffeine Caffeine - pharmacology Caspase Caspases - metabolism Cell death Cell Survival - drug effects Cervical cancer Cervical carcinoma Cervix Cyclic AMP - metabolism Dictyostelium - drug effects Dictyostelium - genetics Dictyostelium - metabolism Drug Resistance Drug Synergism Enzyme Activation - drug effects HeLa Cells Humanities and Social Sciences Humans Intracellular signalling Mortality multidisciplinary Overdose Phospholipase A2 Phospholipases A2 - metabolism Science Signal Transduction - drug effects Survival |
| title | Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death |
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