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Deficiency of PDK1 in cardiac muscle results in heart failure and increased sensitivity to hypoxia
We employed Cre/loxP technology to generate mPDK1 −/− mice, which lack PDK1 in cardiac muscle. Insulin did not activate PKB and S6K, nor did it stimulate 6‐phosphofructo‐2‐kinase and production of fructose 2,6‐bisphosphate, in the hearts of mPDK1 −/− mice, consistent with PDK1 mediating these proces...
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| Published in: | The EMBO journal 2003-09, Vol.22 (18), p.4666-4676 |
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| Main Authors: | , , , , , , , , , , , |
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| container_end_page | 4676 |
| container_issue | 18 |
| container_start_page | 4666 |
| container_title | The EMBO journal |
| container_volume | 22 |
| creator | Mora, Alfonso Davies, Anthony M. Bertrand, Luc Sharif, Isam Budas, Grant R. Jovanović, Sofija Mouton, Véronique Kahn, C. Ronald Lucocq, John M. Gray, Gillian A. Jovanović, Aleksandar Alessi, Dario R. |
| description | We employed Cre/loxP technology to generate mPDK1
−/−
mice, which lack PDK1 in cardiac muscle. Insulin did not activate PKB and S6K, nor did it stimulate 6‐phosphofructo‐2‐kinase and production of fructose 2,6‐bisphosphate, in the hearts of mPDK1
−/−
mice, consistent with PDK1 mediating these processes. All mPDK1
−/−
mice died suddenly between 5 and 11 weeks of age. The mPDK1
−/−
animals had thinner ventricular walls, enlarged atria and right ventricles. Moreover, mPDK1
−/−
muscle mass was markedly reduced due to a reduction in cardiomyocyte volume rather than cardiomyocyte cell number, and markers of heart failure were elevated. These results suggested mPDK1
−/−
mice died of heart failure, a conclusion supported by echocardiographic analysis. By employing a single‐cell assay we found that cardiomyocytes from mPDK1
−/−
mice are markedly more sensitive to hypoxia. These results establish that the PDK1 signalling network plays an important role in regulating cardiac viability and preventing heart failure. They also suggest that a deficiency of the PDK1 pathway might contribute to development of cardiac disease in humans. |
| doi_str_mv | 10.1093/emboj/cdg469 |
| format | article |
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−/−
mice, which lack PDK1 in cardiac muscle. Insulin did not activate PKB and S6K, nor did it stimulate 6‐phosphofructo‐2‐kinase and production of fructose 2,6‐bisphosphate, in the hearts of mPDK1
−/−
mice, consistent with PDK1 mediating these processes. All mPDK1
−/−
mice died suddenly between 5 and 11 weeks of age. The mPDK1
−/−
animals had thinner ventricular walls, enlarged atria and right ventricles. Moreover, mPDK1
−/−
muscle mass was markedly reduced due to a reduction in cardiomyocyte volume rather than cardiomyocyte cell number, and markers of heart failure were elevated. These results suggested mPDK1
−/−
mice died of heart failure, a conclusion supported by echocardiographic analysis. By employing a single‐cell assay we found that cardiomyocytes from mPDK1
−/−
mice are markedly more sensitive to hypoxia. These results establish that the PDK1 signalling network plays an important role in regulating cardiac viability and preventing heart failure. They also suggest that a deficiency of the PDK1 pathway might contribute to development of cardiac disease in humans.</description><identifier>ISSN: 0261-4189</identifier><identifier>ISSN: 1460-2075</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1093/emboj/cdg469</identifier><identifier>PMID: 12970179</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>3-Phosphoinositide-Dependent Protein Kinases ; Akt ; Animals ; cardiac muscle ; Cell Hypoxia - physiology ; Echocardiography ; EMBO24 ; EMBO37 ; Enzyme Activation ; Heart - physiopathology ; heart failure ; Heart Failure - enzymology ; Heart Failure - genetics ; Hypoxia ; Insulin - pharmacology ; Kinetics ; Mice ; Mice, Knockout ; Muscle Cells - physiology ; Myocardium - pathology ; PDK1 ; Phosphofructokinase-2 - metabolism ; PI 3-kinase ; PKB ; Protein Serine-Threonine Kinases - deficiency ; Protein Serine-Threonine Kinases - genetics ; Protein Serine-Threonine Kinases - metabolism</subject><ispartof>The EMBO journal, 2003-09, Vol.22 (18), p.4666-4676</ispartof><rights>European Molecular Biology Organization 2003</rights><rights>Copyright © 2003 European Molecular Biology Organization</rights><rights>Copyright Oxford University Press(England) Sep 15, 2003</rights><rights>Copyright © 2003 European Molecular Biology Organization 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6478-b3023c06b99cfa6027030e36588b20cf11e9cbc2b76eb5977ba8d4e4a1c482493</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC212735/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC212735/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12970179$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mora, Alfonso</creatorcontrib><creatorcontrib>Davies, Anthony M.</creatorcontrib><creatorcontrib>Bertrand, Luc</creatorcontrib><creatorcontrib>Sharif, Isam</creatorcontrib><creatorcontrib>Budas, Grant R.</creatorcontrib><creatorcontrib>Jovanović, Sofija</creatorcontrib><creatorcontrib>Mouton, Véronique</creatorcontrib><creatorcontrib>Kahn, C. Ronald</creatorcontrib><creatorcontrib>Lucocq, John M.</creatorcontrib><creatorcontrib>Gray, Gillian A.</creatorcontrib><creatorcontrib>Jovanović, Aleksandar</creatorcontrib><creatorcontrib>Alessi, Dario R.</creatorcontrib><title>Deficiency of PDK1 in cardiac muscle results in heart failure and increased sensitivity to hypoxia</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><addtitle>EMBO J</addtitle><description>We employed Cre/loxP technology to generate mPDK1
−/−
mice, which lack PDK1 in cardiac muscle. Insulin did not activate PKB and S6K, nor did it stimulate 6‐phosphofructo‐2‐kinase and production of fructose 2,6‐bisphosphate, in the hearts of mPDK1
−/−
mice, consistent with PDK1 mediating these processes. All mPDK1
−/−
mice died suddenly between 5 and 11 weeks of age. The mPDK1
−/−
animals had thinner ventricular walls, enlarged atria and right ventricles. Moreover, mPDK1
−/−
muscle mass was markedly reduced due to a reduction in cardiomyocyte volume rather than cardiomyocyte cell number, and markers of heart failure were elevated. These results suggested mPDK1
−/−
mice died of heart failure, a conclusion supported by echocardiographic analysis. By employing a single‐cell assay we found that cardiomyocytes from mPDK1
−/−
mice are markedly more sensitive to hypoxia. These results establish that the PDK1 signalling network plays an important role in regulating cardiac viability and preventing heart failure. They also suggest that a deficiency of the PDK1 pathway might contribute to development of cardiac disease in humans.</description><subject>3-Phosphoinositide-Dependent Protein Kinases</subject><subject>Akt</subject><subject>Animals</subject><subject>cardiac muscle</subject><subject>Cell Hypoxia - physiology</subject><subject>Echocardiography</subject><subject>EMBO24</subject><subject>EMBO37</subject><subject>Enzyme Activation</subject><subject>Heart - physiopathology</subject><subject>heart failure</subject><subject>Heart Failure - enzymology</subject><subject>Heart Failure - genetics</subject><subject>Hypoxia</subject><subject>Insulin - pharmacology</subject><subject>Kinetics</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Muscle Cells - physiology</subject><subject>Myocardium - pathology</subject><subject>PDK1</subject><subject>Phosphofructokinase-2 - metabolism</subject><subject>PI 3-kinase</subject><subject>PKB</subject><subject>Protein Serine-Threonine Kinases - deficiency</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><issn>0261-4189</issn><issn>1460-2075</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkktv1DAUhSMEotPCji3IYtEVoX7ErwUL6JRCGQoSUJaW49zMeMhjsJPS_HtSMhrKQ7Cy5Pud42MfJ8kDgp8SrNkR1Hm7PnLFMhP6VjIjmcApxZLfTmaYCpJmROm9ZD_GNcaYK0nuJnuEaomJ1LMkn0PpnYfGDagt0fv5G4J8g5wNhbcO1X10FaAAsa-6eD1ZgQ0dKq2v-gDINsW46QLYCAWK0ETf-UvfDahr0WrYtFfe3kvulLaKcH-7HiSfXp58PH6VLt6dvj5-vkidyKRKc4Ypc1jkWrvSCkwlZhiY4ErlFLuSENAudzSXAnKupcytKjLILHGZoplmB8mzyXfT5zUUDpou2Mpsgq9tGExrvfl10viVWbaXhhIqGR_1h1t9aL_2EDtT--igqmwDbR-NZCJTgsn_gkQpLanIRvDxb-C67UMzPoIhmlMuOGUj9GSCXGhjDFDuEhNsrhs2Pxo2U8Mj_ujmLX_C20pHgE_AN1_B8E8zc_L2xZnkmjOpRl066eIoaZYQboT9e5CHE9_YbvwKu4P-8POxg6vd2IYvRkgmufl8fmrO1cXiYn72wSzYd9fS3gg</recordid><startdate>20030915</startdate><enddate>20030915</enddate><creator>Mora, Alfonso</creator><creator>Davies, Anthony M.</creator><creator>Bertrand, Luc</creator><creator>Sharif, Isam</creator><creator>Budas, Grant R.</creator><creator>Jovanović, Sofija</creator><creator>Mouton, Véronique</creator><creator>Kahn, C. Ronald</creator><creator>Lucocq, John M.</creator><creator>Gray, Gillian A.</creator><creator>Jovanović, Aleksandar</creator><creator>Alessi, Dario R.</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><general>Oxford University Press</general><scope>BSCLL</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20030915</creationdate><title>Deficiency of PDK1 in cardiac muscle results in heart failure and increased sensitivity to hypoxia</title><author>Mora, Alfonso ; Davies, Anthony M. ; Bertrand, Luc ; Sharif, Isam ; Budas, Grant R. ; Jovanović, Sofija ; Mouton, Véronique ; Kahn, C. Ronald ; Lucocq, John M. ; Gray, Gillian A. ; Jovanović, Aleksandar ; Alessi, Dario R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6478-b3023c06b99cfa6027030e36588b20cf11e9cbc2b76eb5977ba8d4e4a1c482493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>3-Phosphoinositide-Dependent Protein Kinases</topic><topic>Akt</topic><topic>Animals</topic><topic>cardiac muscle</topic><topic>Cell Hypoxia - physiology</topic><topic>Echocardiography</topic><topic>EMBO24</topic><topic>EMBO37</topic><topic>Enzyme Activation</topic><topic>Heart - physiopathology</topic><topic>heart failure</topic><topic>Heart Failure - enzymology</topic><topic>Heart Failure - genetics</topic><topic>Hypoxia</topic><topic>Insulin - pharmacology</topic><topic>Kinetics</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Muscle Cells - physiology</topic><topic>Myocardium - pathology</topic><topic>PDK1</topic><topic>Phosphofructokinase-2 - metabolism</topic><topic>PI 3-kinase</topic><topic>PKB</topic><topic>Protein Serine-Threonine Kinases - deficiency</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Protein Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mora, Alfonso</creatorcontrib><creatorcontrib>Davies, Anthony M.</creatorcontrib><creatorcontrib>Bertrand, Luc</creatorcontrib><creatorcontrib>Sharif, Isam</creatorcontrib><creatorcontrib>Budas, Grant R.</creatorcontrib><creatorcontrib>Jovanović, Sofija</creatorcontrib><creatorcontrib>Mouton, Véronique</creatorcontrib><creatorcontrib>Kahn, C. Ronald</creatorcontrib><creatorcontrib>Lucocq, John M.</creatorcontrib><creatorcontrib>Gray, Gillian A.</creatorcontrib><creatorcontrib>Jovanović, Aleksandar</creatorcontrib><creatorcontrib>Alessi, Dario R.</creatorcontrib><collection>Istex</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection (ProQuest Medical & Health Databases)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (ProQuest Medical & Health Databases)</collection><collection>Technology Research Database</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest research library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Earth, Atmospheric & Aquatic Science 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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The EMBO journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mora, Alfonso</au><au>Davies, Anthony M.</au><au>Bertrand, Luc</au><au>Sharif, Isam</au><au>Budas, Grant R.</au><au>Jovanović, Sofija</au><au>Mouton, Véronique</au><au>Kahn, C. Ronald</au><au>Lucocq, John M.</au><au>Gray, Gillian A.</au><au>Jovanović, Aleksandar</au><au>Alessi, Dario R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficiency of PDK1 in cardiac muscle results in heart failure and increased sensitivity to hypoxia</atitle><jtitle>The EMBO journal</jtitle><stitle>EMBO J</stitle><addtitle>EMBO J</addtitle><date>2003-09-15</date><risdate>2003</risdate><volume>22</volume><issue>18</issue><spage>4666</spage><epage>4676</epage><pages>4666-4676</pages><issn>0261-4189</issn><issn>1460-2075</issn><eissn>1460-2075</eissn><coden>EMJODG</coden><abstract>We employed Cre/loxP technology to generate mPDK1
−/−
mice, which lack PDK1 in cardiac muscle. Insulin did not activate PKB and S6K, nor did it stimulate 6‐phosphofructo‐2‐kinase and production of fructose 2,6‐bisphosphate, in the hearts of mPDK1
−/−
mice, consistent with PDK1 mediating these processes. All mPDK1
−/−
mice died suddenly between 5 and 11 weeks of age. The mPDK1
−/−
animals had thinner ventricular walls, enlarged atria and right ventricles. Moreover, mPDK1
−/−
muscle mass was markedly reduced due to a reduction in cardiomyocyte volume rather than cardiomyocyte cell number, and markers of heart failure were elevated. These results suggested mPDK1
−/−
mice died of heart failure, a conclusion supported by echocardiographic analysis. By employing a single‐cell assay we found that cardiomyocytes from mPDK1
−/−
mice are markedly more sensitive to hypoxia. These results establish that the PDK1 signalling network plays an important role in regulating cardiac viability and preventing heart failure. They also suggest that a deficiency of the PDK1 pathway might contribute to development of cardiac disease in humans.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>12970179</pmid><doi>10.1093/emboj/cdg469</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0261-4189 |
| ispartof | The EMBO journal, 2003-09, Vol.22 (18), p.4666-4676 |
| issn | 0261-4189 1460-2075 1460-2075 |
| language | eng |
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| source | PubMed Central (Open Access) |
| subjects | 3-Phosphoinositide-Dependent Protein Kinases Akt Animals cardiac muscle Cell Hypoxia - physiology Echocardiography EMBO24 EMBO37 Enzyme Activation Heart - physiopathology heart failure Heart Failure - enzymology Heart Failure - genetics Hypoxia Insulin - pharmacology Kinetics Mice Mice, Knockout Muscle Cells - physiology Myocardium - pathology PDK1 Phosphofructokinase-2 - metabolism PI 3-kinase PKB Protein Serine-Threonine Kinases - deficiency Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism |
| title | Deficiency of PDK1 in cardiac muscle results in heart failure and increased sensitivity to hypoxia |
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