The Lysophospholipids Sphingosine-1-Phosphate and Lysophosphatidic Acid Enhance Survival during Hypoxia in Neonatal Rat Cardiac Myocytes
The lysophospholipids sphingosine-1-phosphate (S1P) and lysophosphatidic acid (LPA) stimulate cellular proliferation and affect numerous cellular functions by signaling through G protein-coupled endothelial differentiation gene-encoded (Edg) receptors. S1P and LPA also act as survival factors in man...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 2001-09, Vol.33 (9), p.1713-1717 |
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| creator | Karliner, Joel S. Honbo, Norman Summers, Kori Gray, Mary O. Goetzl, Edward J. |
| description | The lysophospholipids sphingosine-1-phosphate (S1P) and lysophosphatidic acid (LPA) stimulate cellular proliferation and affect numerous cellular functions by signaling through G protein-coupled endothelial differentiation gene-encoded (Edg) receptors. S1P and LPA also act as survival factors in many cell types, but have not previously been studied in cardiac myocytes. We incubated neonatal rat cardiac myocytes either in room air/1% CO2(normoxia) or in an atmosphere of 99% N2/1%CO2(hypoxia) at 37°C for 18–20 h in the absence of glucose. Cell viability was measured using a calcein ester green fluorescence assay. Under normoxic conditions 88.7±1.0% of the cells were viable after 18–20 h. Severe hypoxia reduced viability to 61.3±4.3% (n=6, P |
| doi_str_mv | 10.1006/jmcc.2001.1429 |
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S1P and LPA also act as survival factors in many cell types, but have not previously been studied in cardiac myocytes. We incubated neonatal rat cardiac myocytes either in room air/1% CO2(normoxia) or in an atmosphere of 99% N2/1%CO2(hypoxia) at 37°C for 18–20 h in the absence of glucose. Cell viability was measured using a calcein ester green fluorescence assay. Under normoxic conditions 88.7±1.0% of the cells were viable after 18–20 h. Severe hypoxia reduced viability to 61.3±4.3% (n=6, P<0.05). In myocytes preincubated with either 10 μ m S1P or 1 μ m LPA for 2 h, the effects of severe hypoxia on cell viability were prevented resulting in survival equivalent to normoxia. Neither the protein kinase C inhibitor chelethyrine (1 μ m) nor the mitochondrial KATPchannel antagonist 5-hydroxydecanoic acid, (5-HD, 100 μ m) had any effect on myocyte survival during severe hypoxia, but both agents completely abolished the ability of S1P to rescue cardiac myocytes from hypoxic cell death. We also tested the effects of dimethylsphingosine (DMS), which inhibits sphingosine kinase synthesis of S1P. Incubation of neonatal rat cardiac myocytes with 10μ m DMS for 2 h in the presence of serum resulted in 25–30% cell death during 18–20 h of normoxia. DMS-induced cell death was prevented by concurrent preincubation with either S1P or GM-1, a ganglioside that activates sphingosine kinase to increase intracellular levels of S1P. We conclude that both S1P and LPA are cardioprotective for hypoxic neonatal rat ventricular myocytes. S1P acts through cellular membrane receptors by signaling mechanisms involving protein kinase C and mitochondrial KATPchannels. Both endogenous and exogenously applied S1P are effective in preventing cell death induced by inhibition of sphingosine kinase.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.2001.1429</identifier><identifier>PMID: 11549349</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Alkaloids ; Animals ; Animals, Newborn ; Anti-Arrhythmia Agents - pharmacology ; Benzophenanthridines ; Cardioprotection ; Cardiotonic Agents - metabolism ; Cardiotonic Agents - pharmacology ; Cell culture ; Cell Hypoxia - physiology ; Cell Survival - drug effects ; Cell Survival - physiology ; Cells, Cultured ; Culture Media, Serum-Free ; Decanoic Acids - pharmacology ; Enzyme Inhibitors - pharmacology ; Gelsolin - pharmacology ; Heart - drug effects ; Hydroxy Acids - pharmacology ; Hypoxia ; KATPchannels ; Lysophosphatidic acid ; Lysophospholipids ; Lysophospholipids - pharmacology ; Myocardium - cytology ; Neonatal rat cardiac myocytes ; Phenanthridines - pharmacology ; Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor) - metabolism ; Protein kinase C ; Rats ; Rats, Sprague-Dawley ; Sphingosine - analogs & derivatives ; Sphingosine - metabolism ; Sphingosine - pharmacology ; Sphingosine-1-phosphate</subject><ispartof>Journal of molecular and cellular cardiology, 2001-09, Vol.33 (9), p.1713-1717</ispartof><rights>2001 Academic Press</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-577553196087cdff71e2e92fd35e971d8f5e38b437eb33cb4b48a0955c19ed83</citedby><cites>FETCH-LOGICAL-c406t-577553196087cdff71e2e92fd35e971d8f5e38b437eb33cb4b48a0955c19ed83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022282801914294$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11549349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Karliner, Joel S.</creatorcontrib><creatorcontrib>Honbo, Norman</creatorcontrib><creatorcontrib>Summers, Kori</creatorcontrib><creatorcontrib>Gray, Mary O.</creatorcontrib><creatorcontrib>Goetzl, Edward J.</creatorcontrib><title>The Lysophospholipids Sphingosine-1-Phosphate and Lysophosphatidic Acid Enhance Survival during Hypoxia in Neonatal Rat Cardiac Myocytes</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>The lysophospholipids sphingosine-1-phosphate (S1P) and lysophosphatidic acid (LPA) stimulate cellular proliferation and affect numerous cellular functions by signaling through G protein-coupled endothelial differentiation gene-encoded (Edg) receptors. S1P and LPA also act as survival factors in many cell types, but have not previously been studied in cardiac myocytes. We incubated neonatal rat cardiac myocytes either in room air/1% CO2(normoxia) or in an atmosphere of 99% N2/1%CO2(hypoxia) at 37°C for 18–20 h in the absence of glucose. Cell viability was measured using a calcein ester green fluorescence assay. Under normoxic conditions 88.7±1.0% of the cells were viable after 18–20 h. Severe hypoxia reduced viability to 61.3±4.3% (n=6, P<0.05). In myocytes preincubated with either 10 μ m S1P or 1 μ m LPA for 2 h, the effects of severe hypoxia on cell viability were prevented resulting in survival equivalent to normoxia. Neither the protein kinase C inhibitor chelethyrine (1 μ m) nor the mitochondrial KATPchannel antagonist 5-hydroxydecanoic acid, (5-HD, 100 μ m) had any effect on myocyte survival during severe hypoxia, but both agents completely abolished the ability of S1P to rescue cardiac myocytes from hypoxic cell death. We also tested the effects of dimethylsphingosine (DMS), which inhibits sphingosine kinase synthesis of S1P. Incubation of neonatal rat cardiac myocytes with 10μ m DMS for 2 h in the presence of serum resulted in 25–30% cell death during 18–20 h of normoxia. DMS-induced cell death was prevented by concurrent preincubation with either S1P or GM-1, a ganglioside that activates sphingosine kinase to increase intracellular levels of S1P. We conclude that both S1P and LPA are cardioprotective for hypoxic neonatal rat ventricular myocytes. S1P acts through cellular membrane receptors by signaling mechanisms involving protein kinase C and mitochondrial KATPchannels. Both endogenous and exogenously applied S1P are effective in preventing cell death induced by inhibition of sphingosine kinase.</description><subject>Alkaloids</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Benzophenanthridines</subject><subject>Cardioprotection</subject><subject>Cardiotonic Agents - metabolism</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cell culture</subject><subject>Cell Hypoxia - physiology</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>Culture Media, Serum-Free</subject><subject>Decanoic Acids - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Gelsolin - pharmacology</subject><subject>Heart - drug effects</subject><subject>Hydroxy Acids - pharmacology</subject><subject>Hypoxia</subject><subject>KATPchannels</subject><subject>Lysophosphatidic acid</subject><subject>Lysophospholipids</subject><subject>Lysophospholipids - pharmacology</subject><subject>Myocardium - cytology</subject><subject>Neonatal rat cardiac myocytes</subject><subject>Phenanthridines - pharmacology</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - metabolism</subject><subject>Protein kinase C</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sphingosine - analogs & derivatives</subject><subject>Sphingosine - metabolism</subject><subject>Sphingosine - pharmacology</subject><subject>Sphingosine-1-phosphate</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1vEzEQhi0EoqFw5Yh84rbBn1n7WEWlRUqhanO3vPYscbVZL_ZuxP4DfnadJhJcOIzm8D7zSvMg9JGSJSVk9eVp79ySEUKXVDD9Ci0o0bJSUonXaEEIYxVTTF2gdzk_EUK04PwtuqBUCs2FXqA_2x3gzZzjsIu5TBeG4DN-HHah_xlz6KGi1f1LZkfAtvf_0HYMPjh85YLH1_3O9g7w45QO4WA77KdUKvDtPMTfweLQ4-8QezuW6MGOeG2TD9bhuzm6eYT8Hr1pbZfhw3lfou3X6-36ttr8uPm2vtpUTpDVWMm6lpJTvSKqdr5tawoMNGs9l6Br6lUrgatG8Boazl0jGqFsUSId1eAVv0SfT7VDir8myKPZh-yg62wPccqmLmrkirECLk-gSzHnBK0ZUtjbNBtKzFG9Oao3R_XmqL4cfDo3T80e_F_87LoA6gRAee8QIJnsAhRnPiRwo_Ex_K_7GW9IlPY</recordid><startdate>20010901</startdate><enddate>20010901</enddate><creator>Karliner, Joel S.</creator><creator>Honbo, Norman</creator><creator>Summers, Kori</creator><creator>Gray, Mary O.</creator><creator>Goetzl, Edward J.</creator><general>Elsevier Ltd</general><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>20010901</creationdate><title>The Lysophospholipids Sphingosine-1-Phosphate and Lysophosphatidic Acid Enhance Survival during Hypoxia in Neonatal Rat Cardiac Myocytes</title><author>Karliner, Joel S. ; Honbo, Norman ; Summers, Kori ; Gray, Mary O. ; Goetzl, Edward J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-577553196087cdff71e2e92fd35e971d8f5e38b437eb33cb4b48a0955c19ed83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Alkaloids</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Benzophenanthridines</topic><topic>Cardioprotection</topic><topic>Cardiotonic Agents - metabolism</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cell culture</topic><topic>Cell Hypoxia - physiology</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Cells, Cultured</topic><topic>Culture Media, Serum-Free</topic><topic>Decanoic Acids - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Gelsolin - pharmacology</topic><topic>Heart - drug effects</topic><topic>Hydroxy Acids - pharmacology</topic><topic>Hypoxia</topic><topic>KATPchannels</topic><topic>Lysophosphatidic acid</topic><topic>Lysophospholipids</topic><topic>Lysophospholipids - pharmacology</topic><topic>Myocardium - cytology</topic><topic>Neonatal rat cardiac myocytes</topic><topic>Phenanthridines - pharmacology</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - metabolism</topic><topic>Protein kinase C</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sphingosine - analogs & derivatives</topic><topic>Sphingosine - metabolism</topic><topic>Sphingosine - pharmacology</topic><topic>Sphingosine-1-phosphate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Karliner, Joel S.</creatorcontrib><creatorcontrib>Honbo, Norman</creatorcontrib><creatorcontrib>Summers, Kori</creatorcontrib><creatorcontrib>Gray, Mary O.</creatorcontrib><creatorcontrib>Goetzl, Edward J.</creatorcontrib><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>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Karliner, Joel S.</au><au>Honbo, Norman</au><au>Summers, Kori</au><au>Gray, Mary O.</au><au>Goetzl, Edward J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Lysophospholipids Sphingosine-1-Phosphate and Lysophosphatidic Acid Enhance Survival during Hypoxia in Neonatal Rat Cardiac Myocytes</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>2001-09-01</date><risdate>2001</risdate><volume>33</volume><issue>9</issue><spage>1713</spage><epage>1717</epage><pages>1713-1717</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>The lysophospholipids sphingosine-1-phosphate (S1P) and lysophosphatidic acid (LPA) stimulate cellular proliferation and affect numerous cellular functions by signaling through G protein-coupled endothelial differentiation gene-encoded (Edg) receptors. S1P and LPA also act as survival factors in many cell types, but have not previously been studied in cardiac myocytes. We incubated neonatal rat cardiac myocytes either in room air/1% CO2(normoxia) or in an atmosphere of 99% N2/1%CO2(hypoxia) at 37°C for 18–20 h in the absence of glucose. Cell viability was measured using a calcein ester green fluorescence assay. Under normoxic conditions 88.7±1.0% of the cells were viable after 18–20 h. Severe hypoxia reduced viability to 61.3±4.3% (n=6, P<0.05). In myocytes preincubated with either 10 μ m S1P or 1 μ m LPA for 2 h, the effects of severe hypoxia on cell viability were prevented resulting in survival equivalent to normoxia. Neither the protein kinase C inhibitor chelethyrine (1 μ m) nor the mitochondrial KATPchannel antagonist 5-hydroxydecanoic acid, (5-HD, 100 μ m) had any effect on myocyte survival during severe hypoxia, but both agents completely abolished the ability of S1P to rescue cardiac myocytes from hypoxic cell death. We also tested the effects of dimethylsphingosine (DMS), which inhibits sphingosine kinase synthesis of S1P. Incubation of neonatal rat cardiac myocytes with 10μ m DMS for 2 h in the presence of serum resulted in 25–30% cell death during 18–20 h of normoxia. DMS-induced cell death was prevented by concurrent preincubation with either S1P or GM-1, a ganglioside that activates sphingosine kinase to increase intracellular levels of S1P. We conclude that both S1P and LPA are cardioprotective for hypoxic neonatal rat ventricular myocytes. S1P acts through cellular membrane receptors by signaling mechanisms involving protein kinase C and mitochondrial KATPchannels. Both endogenous and exogenously applied S1P are effective in preventing cell death induced by inhibition of sphingosine kinase.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>11549349</pmid><doi>10.1006/jmcc.2001.1429</doi><tpages>5</tpages></addata></record> |
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| ispartof | Journal of molecular and cellular cardiology, 2001-09, Vol.33 (9), p.1713-1717 |
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| subjects | Alkaloids Animals Animals, Newborn Anti-Arrhythmia Agents - pharmacology Benzophenanthridines Cardioprotection Cardiotonic Agents - metabolism Cardiotonic Agents - pharmacology Cell culture Cell Hypoxia - physiology Cell Survival - drug effects Cell Survival - physiology Cells, Cultured Culture Media, Serum-Free Decanoic Acids - pharmacology Enzyme Inhibitors - pharmacology Gelsolin - pharmacology Heart - drug effects Hydroxy Acids - pharmacology Hypoxia KATPchannels Lysophosphatidic acid Lysophospholipids Lysophospholipids - pharmacology Myocardium - cytology Neonatal rat cardiac myocytes Phenanthridines - pharmacology Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors Phosphotransferases (Alcohol Group Acceptor) - metabolism Protein kinase C Rats Rats, Sprague-Dawley Sphingosine - analogs & derivatives Sphingosine - metabolism Sphingosine - pharmacology Sphingosine-1-phosphate |
| title | The Lysophospholipids Sphingosine-1-Phosphate and Lysophosphatidic Acid Enhance Survival during Hypoxia in Neonatal Rat Cardiac Myocytes |
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