TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70
The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H 2 O 2 )-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H 2 O 2 . We observed a significant AMPK activation in H 2 O 2 -treated...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2013-05, Vol.377 (1-2), p.35-44 |
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| creator | Chen, Zhiyu Shen, Xiaolu Shen, Fengyan Zhong, Wei Wu, Hai Liu, Sha Lai, Jiang |
| description | The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H
2
O
2
)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H
2
O
2
. We observed a significant AMPK activation in H
2
O
2
-treated cardiomyocytes (both primary cells and H9c2 line). Inhibition of AMPK by its inhibitor or RNAi-reduced H
2
O
2
-induced cardiomyocyte death. We here proposed that transforming growth factor-β-activating kinase 1 (TAK1) might be the upstream kinase for AMPK activation by H
2
O
2
. H
2
O
2
-induced TAK1 activation, which recruited and activated AMPK. TAK1 inhibitor significantly suppressed H
2
O
2
-induced AMPK activation and following cardiomyocyte death, while over-expression of TAK1-facilitated AMPK activation and aggregated cardiomyocyte death. Importantly, heat shock protein-70 (HSP-70)-reduced H
2
O
2
-induced reactive oxygen species (ROS) accumulation, the TAK1/AMPK activation and cardiomyocyte death. In conclusion, we here suggest that TAK1 activates AMPK-dependent cell death pathway in H
2
O
2
-treated cardiomyocytes, and HSP-70 inhibits the signaling pathway by reducing ROS content. |
| doi_str_mv | 10.1007/s11010-013-1568-z |
| format | Article |
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2
O
2
)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H
2
O
2
. We observed a significant AMPK activation in H
2
O
2
-treated cardiomyocytes (both primary cells and H9c2 line). Inhibition of AMPK by its inhibitor or RNAi-reduced H
2
O
2
-induced cardiomyocyte death. We here proposed that transforming growth factor-β-activating kinase 1 (TAK1) might be the upstream kinase for AMPK activation by H
2
O
2
. H
2
O
2
-induced TAK1 activation, which recruited and activated AMPK. TAK1 inhibitor significantly suppressed H
2
O
2
-induced AMPK activation and following cardiomyocyte death, while over-expression of TAK1-facilitated AMPK activation and aggregated cardiomyocyte death. Importantly, heat shock protein-70 (HSP-70)-reduced H
2
O
2
-induced reactive oxygen species (ROS) accumulation, the TAK1/AMPK activation and cardiomyocyte death. In conclusion, we here suggest that TAK1 activates AMPK-dependent cell death pathway in H
2
O
2
-treated cardiomyocytes, and HSP-70 inhibits the signaling pathway by reducing ROS content.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-013-1568-z</identifier><identifier>PMID: 23378049</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenylate Kinase - metabolism ; Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Bone morphogenetic proteins ; Cardiology ; Cardiomyocytes ; Cell death ; Cell Line ; Cell Survival ; Enzyme Activation ; Heart cells ; Heat shock proteins ; HSP70 Heat-Shock Proteins - physiology ; Hydrogen peroxide ; Hydrogen Peroxide - pharmacology ; Lactones - pharmacology ; Life Sciences ; MAP Kinase Kinase Kinases - antagonists & inhibitors ; MAP Kinase Kinase Kinases - physiology ; Medical Biochemistry ; Mortality ; Myocytes, Cardiac - enzymology ; Myocytes, Cardiac - physiology ; Oncology ; Oxidants - pharmacology ; Primary Cell Culture ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Resorcinols - pharmacology ; Signal Transduction ; Toy industry</subject><ispartof>Molecular and cellular biochemistry, 2013-05, Vol.377 (1-2), p.35-44</ispartof><rights>Springer Science+Business Media New York 2013</rights><rights>COPYRIGHT 2013 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c605t-b2c6a0feb267c4e000458b480eb693ccc573fc44792a713ff5cca0a13b07b1a73</citedby><cites>FETCH-LOGICAL-c605t-b2c6a0feb267c4e000458b480eb693ccc573fc44792a713ff5cca0a13b07b1a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-013-1568-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-013-1568-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23378049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Zhiyu</creatorcontrib><creatorcontrib>Shen, Xiaolu</creatorcontrib><creatorcontrib>Shen, Fengyan</creatorcontrib><creatorcontrib>Zhong, Wei</creatorcontrib><creatorcontrib>Wu, Hai</creatorcontrib><creatorcontrib>Liu, Sha</creatorcontrib><creatorcontrib>Lai, Jiang</creatorcontrib><title>TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H
2
O
2
)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H
2
O
2
. We observed a significant AMPK activation in H
2
O
2
-treated cardiomyocytes (both primary cells and H9c2 line). Inhibition of AMPK by its inhibitor or RNAi-reduced H
2
O
2
-induced cardiomyocyte death. We here proposed that transforming growth factor-β-activating kinase 1 (TAK1) might be the upstream kinase for AMPK activation by H
2
O
2
. H
2
O
2
-induced TAK1 activation, which recruited and activated AMPK. TAK1 inhibitor significantly suppressed H
2
O
2
-induced AMPK activation and following cardiomyocyte death, while over-expression of TAK1-facilitated AMPK activation and aggregated cardiomyocyte death. Importantly, heat shock protein-70 (HSP-70)-reduced H
2
O
2
-induced reactive oxygen species (ROS) accumulation, the TAK1/AMPK activation and cardiomyocyte death. In conclusion, we here suggest that TAK1 activates AMPK-dependent cell death pathway in H
2
O
2
-treated cardiomyocytes, and HSP-70 inhibits the signaling pathway by reducing ROS content.</description><subject>Adenylate Kinase - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Bone morphogenetic proteins</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Enzyme Activation</subject><subject>Heart cells</subject><subject>Heat shock proteins</subject><subject>HSP70 Heat-Shock Proteins - physiology</subject><subject>Hydrogen peroxide</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Lactones - pharmacology</subject><subject>Life Sciences</subject><subject>MAP Kinase Kinase Kinases - antagonists & inhibitors</subject><subject>MAP Kinase Kinase Kinases - physiology</subject><subject>Medical Biochemistry</subject><subject>Mortality</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Oncology</subject><subject>Oxidants - pharmacology</subject><subject>Primary Cell Culture</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Resorcinols - pharmacology</subject><subject>Signal Transduction</subject><subject>Toy industry</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkkFv1DAQhSMEokvhB3BBlrjiMhM7cXJcVVBQi-BQzpbjTDYumzjYWSA99afj1RYoEiBkyZbs772Rn16WPUU4QQD1MiICAgcUHIuy4tf3shUWSnBZY30_W4EA4BUqdZQ9ivEKEgyID7OjXAhVgaxX2c3l-hyZsbP7YmaKbP3uwzlvaaKxpXFmlrZb1pKZezal7atZmBtZv7TBb2hkEwX_zbXE55AYapk1oXV-WLxdktuLBPeucfuXZmF9Yljsvf3EpuBnciNX8Dh70JltpCe353H28fWry9M3_OL92dvT9QW3JRQzb3JbGuioyUtlJQGALKpGVkBNWQtrbfp2Z6VUdW4Uiq4rrDVgUDSgGjRKHGfPD75p9OcdxVlf-V0Y00iNIoVXqVqIX9TGbEm7sfNzMHZw0eq1lHWhFEr8JyVEmQLHfO918gcqrZYGZ_1InUv3v9n-l-DuBDwIbPAxBur0FNxgwqIR9L4h-tAQnRqi9w3R10nz7DaHXTNQ-1PxoxIJyA9ATE_jhsKdoP7q-h0JcMRP</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Chen, Zhiyu</creator><creator>Shen, Xiaolu</creator><creator>Shen, Fengyan</creator><creator>Zhong, Wei</creator><creator>Wu, Hai</creator><creator>Liu, Sha</creator><creator>Lai, Jiang</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</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>88I</scope><scope>8AO</scope><scope>8FD</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20130501</creationdate><title>TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70</title><author>Chen, Zhiyu ; Shen, Xiaolu ; Shen, Fengyan ; Zhong, Wei ; Wu, Hai ; Liu, Sha ; Lai, Jiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c605t-b2c6a0feb267c4e000458b480eb693ccc573fc44792a713ff5cca0a13b07b1a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenylate Kinase - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Bone morphogenetic proteins</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cell death</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Enzyme Activation</topic><topic>Heart cells</topic><topic>Heat shock proteins</topic><topic>HSP70 Heat-Shock Proteins - physiology</topic><topic>Hydrogen peroxide</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Lactones - pharmacology</topic><topic>Life Sciences</topic><topic>MAP Kinase Kinase Kinases - antagonists & inhibitors</topic><topic>MAP Kinase Kinase Kinases - physiology</topic><topic>Medical Biochemistry</topic><topic>Mortality</topic><topic>Myocytes, Cardiac - enzymology</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Oncology</topic><topic>Oxidants - pharmacology</topic><topic>Primary Cell Culture</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Resorcinols - pharmacology</topic><topic>Signal Transduction</topic><topic>Toy industry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Zhiyu</creatorcontrib><creatorcontrib>Shen, Xiaolu</creatorcontrib><creatorcontrib>Shen, Fengyan</creatorcontrib><creatorcontrib>Zhong, Wei</creatorcontrib><creatorcontrib>Wu, Hai</creatorcontrib><creatorcontrib>Liu, Sha</creatorcontrib><creatorcontrib>Lai, Jiang</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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</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 Pharma Collection</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>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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Zhiyu</au><au>Shen, Xiaolu</au><au>Shen, Fengyan</au><au>Zhong, Wei</au><au>Wu, Hai</au><au>Liu, Sha</au><au>Lai, Jiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>377</volume><issue>1-2</issue><spage>35</spage><epage>44</epage><pages>35-44</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H
2
O
2
)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H
2
O
2
. We observed a significant AMPK activation in H
2
O
2
-treated cardiomyocytes (both primary cells and H9c2 line). Inhibition of AMPK by its inhibitor or RNAi-reduced H
2
O
2
-induced cardiomyocyte death. We here proposed that transforming growth factor-β-activating kinase 1 (TAK1) might be the upstream kinase for AMPK activation by H
2
O
2
. H
2
O
2
-induced TAK1 activation, which recruited and activated AMPK. TAK1 inhibitor significantly suppressed H
2
O
2
-induced AMPK activation and following cardiomyocyte death, while over-expression of TAK1-facilitated AMPK activation and aggregated cardiomyocyte death. Importantly, heat shock protein-70 (HSP-70)-reduced H
2
O
2
-induced reactive oxygen species (ROS) accumulation, the TAK1/AMPK activation and cardiomyocyte death. In conclusion, we here suggest that TAK1 activates AMPK-dependent cell death pathway in H
2
O
2
-treated cardiomyocytes, and HSP-70 inhibits the signaling pathway by reducing ROS content.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>23378049</pmid><doi>10.1007/s11010-013-1568-z</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Molecular and cellular biochemistry, 2013-05, Vol.377 (1-2), p.35-44 |
| issn | 0300-8177 1573-4919 |
| language | eng |
| recordid | cdi_proquest_journals_1356887933 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Adenylate Kinase - metabolism Animals Apoptosis Biochemistry Biomedical and Life Sciences Bone morphogenetic proteins Cardiology Cardiomyocytes Cell death Cell Line Cell Survival Enzyme Activation Heart cells Heat shock proteins HSP70 Heat-Shock Proteins - physiology Hydrogen peroxide Hydrogen Peroxide - pharmacology Lactones - pharmacology Life Sciences MAP Kinase Kinase Kinases - antagonists & inhibitors MAP Kinase Kinase Kinases - physiology Medical Biochemistry Mortality Myocytes, Cardiac - enzymology Myocytes, Cardiac - physiology Oncology Oxidants - pharmacology Primary Cell Culture Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Resorcinols - pharmacology Signal Transduction Toy industry |
| title | TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70 |
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