Cyclic AMP is both a pro-apoptotic and anti-apoptotic second messenger
The second messenger cyclic AMP (cAMP) can either stimulate or inhibit programmed cell death (apoptosis). Here, we review examples of cell types that show pro‐apoptotic or anti‐apoptotic responses to increases in cAMP. We also show that cells can have both such responses, although predominantly havi...
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| Veröffentlicht in: | Acta Physiologica 2012-02, Vol.204 (2), p.277-287 |
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| creator | Insel, P. A. Zhang, L. Murray, F. Yokouchi, H. Zambon, A. C. |
| description | The second messenger cyclic AMP (cAMP) can either stimulate or inhibit programmed cell death (apoptosis). Here, we review examples of cell types that show pro‐apoptotic or anti‐apoptotic responses to increases in cAMP. We also show that cells can have both such responses, although predominantly having one or the other. Protein kinase A (PKA)‐promoted changes in phosphorylation and gene expression can mediate pro‐apoptotic responses, such as in murine S49 lymphoma cells, based on evidence that mutants lacking PKA fail to undergo cAMP‐promoted, mitochondria‐dependent apoptosis. Mechanisms for the anti‐apoptotic response to cAMP likely involve Epac (Exchange protein activated by cAMP), a cAMP‐regulated effector that is a guanine nucleotide exchange factor (GEF) for the low molecular weight G‐protein, Rap1. Therapeutic approaches that activate PKA‐mediated pro‐apoptosis or block Epac‐mediated anti‐apoptotisis may provide a means to enhance cell killing, such as in certain cancers. In contrast, efforts to block PKA or stimulate Epac have the potential to be useful in diseases settings (such as heart failure) associated with cAMP‐promoted apoptosis. |
| doi_str_mv | 10.1111/j.1748-1716.2011.02273.x |
| format | Article |
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A. ; Zhang, L. ; Murray, F. ; Yokouchi, H. ; Zambon, A. C.</creator><creatorcontrib>Insel, P. A. ; Zhang, L. ; Murray, F. ; Yokouchi, H. ; Zambon, A. C.</creatorcontrib><description>The second messenger cyclic AMP (cAMP) can either stimulate or inhibit programmed cell death (apoptosis). Here, we review examples of cell types that show pro‐apoptotic or anti‐apoptotic responses to increases in cAMP. We also show that cells can have both such responses, although predominantly having one or the other. Protein kinase A (PKA)‐promoted changes in phosphorylation and gene expression can mediate pro‐apoptotic responses, such as in murine S49 lymphoma cells, based on evidence that mutants lacking PKA fail to undergo cAMP‐promoted, mitochondria‐dependent apoptosis. Mechanisms for the anti‐apoptotic response to cAMP likely involve Epac (Exchange protein activated by cAMP), a cAMP‐regulated effector that is a guanine nucleotide exchange factor (GEF) for the low molecular weight G‐protein, Rap1. Therapeutic approaches that activate PKA‐mediated pro‐apoptosis or block Epac‐mediated anti‐apoptotisis may provide a means to enhance cell killing, such as in certain cancers. In contrast, efforts to block PKA or stimulate Epac have the potential to be useful in diseases settings (such as heart failure) associated with cAMP‐promoted apoptosis.</description><identifier>ISSN: 1748-1708</identifier><identifier>EISSN: 1748-1716</identifier><identifier>DOI: 10.1111/j.1748-1716.2011.02273.x</identifier><identifier>PMID: 21385327</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Apoptosis ; Apoptosis Regulatory Proteins - metabolism ; Biological and medical sciences ; Cyclic AMP - metabolism ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Epac ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Guanine Nucleotide Exchange Factors - metabolism ; Kinases ; Mitochondria - metabolism ; Phosphorylation - physiology ; protein kinase A ; Proteins ; Rap1 ; rap1 GTP-Binding Proteins - metabolism ; S49 cell ; Second Messenger Systems - physiology ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Acta Physiologica, 2012-02, Vol.204 (2), p.277-287</ispartof><rights>2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society</rights><rights>2015 INIST-CNRS</rights><rights>2011 The Authors. 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A.</creatorcontrib><creatorcontrib>Zhang, L.</creatorcontrib><creatorcontrib>Murray, F.</creatorcontrib><creatorcontrib>Yokouchi, H.</creatorcontrib><creatorcontrib>Zambon, A. C.</creatorcontrib><title>Cyclic AMP is both a pro-apoptotic and anti-apoptotic second messenger</title><title>Acta Physiologica</title><addtitle>Acta Physiol (Oxf)</addtitle><description>The second messenger cyclic AMP (cAMP) can either stimulate or inhibit programmed cell death (apoptosis). Here, we review examples of cell types that show pro‐apoptotic or anti‐apoptotic responses to increases in cAMP. We also show that cells can have both such responses, although predominantly having one or the other. Protein kinase A (PKA)‐promoted changes in phosphorylation and gene expression can mediate pro‐apoptotic responses, such as in murine S49 lymphoma cells, based on evidence that mutants lacking PKA fail to undergo cAMP‐promoted, mitochondria‐dependent apoptosis. Mechanisms for the anti‐apoptotic response to cAMP likely involve Epac (Exchange protein activated by cAMP), a cAMP‐regulated effector that is a guanine nucleotide exchange factor (GEF) for the low molecular weight G‐protein, Rap1. Therapeutic approaches that activate PKA‐mediated pro‐apoptosis or block Epac‐mediated anti‐apoptotisis may provide a means to enhance cell killing, such as in certain cancers. In contrast, efforts to block PKA or stimulate Epac have the potential to be useful in diseases settings (such as heart failure) associated with cAMP‐promoted apoptosis.</description><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cyclic AMP - metabolism</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Epac</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Guanine Nucleotide Exchange Factors - metabolism</subject><subject>Kinases</subject><subject>Mitochondria - metabolism</subject><subject>Phosphorylation - physiology</subject><subject>protein kinase A</subject><subject>Proteins</subject><subject>Rap1</subject><subject>rap1 GTP-Binding Proteins - metabolism</subject><subject>S49 cell</subject><subject>Second Messenger Systems - physiology</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>1748-1708</issn><issn>1748-1716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUV1v1DAQjBCIVqV_AUVCiKek_ojt-AXpdOJapJZWpcDjynGc1kcuTu0c3P37Or0jLTxhaeXVzuxodydJUoxyHN_JMseiKDMsMM8JwjhHhAiab14khxPwcspReZAch7BECGGCaUHI6-QgJiWjRBwmi_lWt1ans4ur1Ia0csNdqtLeu0z1rh_cEDHV1TEG-6wUjHaxujIhmO7W-DfJq0a1wRzv_6Pk2-LTzfwsO788_TyfnWeaU06zslaVqStTYS4Fk7iuG0WZYVwzjoRCvJa8MkwLVuESyUKVNTdYmqaRUquqokfJx51uv65WptamG7xqofd2pfwWnLLwN9LZO7h1v4BiwgpCo8CHvYB392sTBljZoE3bqs64dQCJCy6w4DIy3_3DXLq17-J2EHGBOCnlqFfuWNq7ELxpplkwgtEuWMLoBIyuwGgXPNoFm9j69vkuU-MfcyLh_Z6gglZt41WnbXjisXhSJMXTUX7b1mz_ewCYXZ3NxjQKZDsBGwazmQSU_wlcUMHgx5dT-F4UxVe-uIFr-gAMfL_h</recordid><startdate>201202</startdate><enddate>201202</enddate><creator>Insel, P. A.</creator><creator>Zhang, L.</creator><creator>Murray, F.</creator><creator>Yokouchi, H.</creator><creator>Zambon, A. C.</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7TK</scope><scope>7TS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201202</creationdate><title>Cyclic AMP is both a pro-apoptotic and anti-apoptotic second messenger</title><author>Insel, P. A. ; Zhang, L. ; Murray, F. ; Yokouchi, H. ; Zambon, A. C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6363-8dabedbeb1697591ddfa35e56c5607a06d96be5c75b18094a8d6e19eff99cabb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cyclic AMP - metabolism</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Epac</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Guanine Nucleotide Exchange Factors - metabolism</topic><topic>Kinases</topic><topic>Mitochondria - metabolism</topic><topic>Phosphorylation - physiology</topic><topic>protein kinase A</topic><topic>Proteins</topic><topic>Rap1</topic><topic>rap1 GTP-Binding Proteins - metabolism</topic><topic>S49 cell</topic><topic>Second Messenger Systems - physiology</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Insel, P. A.</creatorcontrib><creatorcontrib>Zhang, L.</creatorcontrib><creatorcontrib>Murray, F.</creatorcontrib><creatorcontrib>Yokouchi, H.</creatorcontrib><creatorcontrib>Zambon, A. 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C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclic AMP is both a pro-apoptotic and anti-apoptotic second messenger</atitle><jtitle>Acta Physiologica</jtitle><addtitle>Acta Physiol (Oxf)</addtitle><date>2012-02</date><risdate>2012</risdate><volume>204</volume><issue>2</issue><spage>277</spage><epage>287</epage><pages>277-287</pages><issn>1748-1708</issn><eissn>1748-1716</eissn><abstract>The second messenger cyclic AMP (cAMP) can either stimulate or inhibit programmed cell death (apoptosis). Here, we review examples of cell types that show pro‐apoptotic or anti‐apoptotic responses to increases in cAMP. We also show that cells can have both such responses, although predominantly having one or the other. Protein kinase A (PKA)‐promoted changes in phosphorylation and gene expression can mediate pro‐apoptotic responses, such as in murine S49 lymphoma cells, based on evidence that mutants lacking PKA fail to undergo cAMP‐promoted, mitochondria‐dependent apoptosis. Mechanisms for the anti‐apoptotic response to cAMP likely involve Epac (Exchange protein activated by cAMP), a cAMP‐regulated effector that is a guanine nucleotide exchange factor (GEF) for the low molecular weight G‐protein, Rap1. Therapeutic approaches that activate PKA‐mediated pro‐apoptosis or block Epac‐mediated anti‐apoptotisis may provide a means to enhance cell killing, such as in certain cancers. 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| subjects | Apoptosis Apoptosis Regulatory Proteins - metabolism Biological and medical sciences Cyclic AMP - metabolism Cyclic AMP-Dependent Protein Kinases - metabolism Epac Fundamental and applied biological sciences. Psychology Gene expression Guanine Nucleotide Exchange Factors - metabolism Kinases Mitochondria - metabolism Phosphorylation - physiology protein kinase A Proteins Rap1 rap1 GTP-Binding Proteins - metabolism S49 cell Second Messenger Systems - physiology Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Cyclic AMP is both a pro-apoptotic and anti-apoptotic second messenger |
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