A direct requirement of nuclear factor-kappa B for suppression of apoptosis in ventricular myocytes
Faculty of Medicine, Department of Physiology, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6 Nuclear factor- B (NF- B) is a ubiquitously expressed cellular factor regulated by the cytoplasmic factor inh...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2000-09, Vol.279 (3), p.H939-H945 |
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| container_issue | 3 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 279 |
| creator | Mustapha, Shareef Kirshner, Alla De Moissac, Danielle Kirshenbaum, Lorrie A |
| description | Faculty of Medicine, Department of Physiology, Institute of
Cardiovascular Sciences, St. Boniface General Hospital Research Centre,
University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6
Nuclear factor- B
(NF- B) is a ubiquitously expressed cellular factor regulated by the
cytoplasmic factor inhibitor protein B (I B ). Activation of
NF- B by cytokines, including tumor necrosis factor- (TNF- ),
requires the phosphorylation and degradation of I B . An
anti-apoptotic role for NF- B has recently been suggested. In
the present study, we ascertained whether death-promoting signals and
apoptosis mediated by TNF- are suppressed by NF- B in postnatal ventricular myocytes. Stimulation of myocytes with TNF- resulted in
a 12.1-fold increase ( P |
| doi_str_mv | 10.1152/ajpheart.2000.279.3.H939 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_highw</sourceid><recordid>TN_cdi_highwire_physiology_ajpheart_279_3_H939</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10993753</sourcerecordid><originalsourceid>FETCH-LOGICAL-c401t-df978295c9492ddca2546933cca30396096d27de3bc49326f5987ef9e613a3713</originalsourceid><addsrcrecordid>eNp1kF1PwyAUhonRuDn9C4Y_0AqctR3eTeOcyRJv5jVhFLbObiC0av-9NPNjN15xEt7nPTkPQpiSlNKM3cit22jpm5QRQlJW8BTSOQd-gobxmyU0A36KhgRySHIK2QBdhLCN2azI4RwNKOEcigyGSE1xWXmtGuz1Wxunnd432Bq8b1UdV2AjVWN98iqdk_gOG-txaJ3zOoTK7vukdNY1NlQBV3v8HnFfqbaO6K6zqmt0uERnRtZBX32_I_Qye1jez5PF8-PT_XSRqDGhTVIaXkwYzxQfc1aWSrJsnHMApSQQ4DnhecmKUsNKjTmw3GR8UmjDdbxQQkFhhCaHXuVtCF4b4Xy1k74TlIjem_jxJnpvInoTIHpvEb0-oK5d7XR5BB5ExUB6CGyq9eYjehJu00UDtV13R7XHjbf_A7O2rpf6s_kl_0DhSgNfCruTwQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>A direct requirement of nuclear factor-kappa B for suppression of apoptosis in ventricular myocytes</title><source>MEDLINE</source><source>American Physiological Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Mustapha, Shareef ; Kirshner, Alla ; De Moissac, Danielle ; Kirshenbaum, Lorrie A</creator><creatorcontrib>Mustapha, Shareef ; Kirshner, Alla ; De Moissac, Danielle ; Kirshenbaum, Lorrie A</creatorcontrib><description>Faculty of Medicine, Department of Physiology, Institute of
Cardiovascular Sciences, St. Boniface General Hospital Research Centre,
University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6
Nuclear factor- B
(NF- B) is a ubiquitously expressed cellular factor regulated by the
cytoplasmic factor inhibitor protein B (I B ). Activation of
NF- B by cytokines, including tumor necrosis factor- (TNF- ),
requires the phosphorylation and degradation of I B . An
anti-apoptotic role for NF- B has recently been suggested. In
the present study, we ascertained whether death-promoting signals and
apoptosis mediated by TNF- are suppressed by NF- B in postnatal ventricular myocytes. Stimulation of myocytes with TNF- resulted in
a 12.1-fold increase ( P < 0.01) in NF- B-dependent
gene transcription and DNA binding compared with controls. This was
accompanied by a corresponding increase in the NF- B target protein
A20 as determined by Western blot analysis. Vital staining revealed
that TNF- was not cytotoxic to myocytes and did not provoke
apoptosis. Adenovirus-mediated delivery of a nonphosphorylatable form
of I B to inactivate NF- B prevented TNF- -stimulated
NF- B-dependent gene transcription and nuclear NF- B DNA binding.
Importantly, myocytes stimulated with TNF- and defective for NF- B
activation resulted in a 2.2-fold increase ( P < 0.001)
in apoptosis. To our knowledge, the data provide the first indication
that a functional NF- B signaling pathway is crucial for suppressing
death-promoting signals mediated by TNF- in ventricular myocytes.
adenovirus; inflammation; cytokines; heart failure</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.2000.279.3.H939</identifier><identifier>PMID: 10993753</identifier><language>eng</language><publisher>United States</publisher><subject>Adenoviridae - genetics ; Animals ; Apoptosis - drug effects ; Cell Count - drug effects ; Cell Survival - drug effects ; Cells, Cultured ; Ceramides - pharmacology ; Coloring Agents ; DNA Fragmentation - drug effects ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Genes, Reporter - genetics ; Heart Ventricles - cytology ; Heart Ventricles - drug effects ; Heart Ventricles - metabolism ; I-kappa B Proteins ; Mutagenesis, Site-Directed ; Myocardium - cytology ; Myocardium - metabolism ; NF-kappa B - metabolism ; NF-kappa B - pharmacology ; NF-KappaB Inhibitor alpha ; Proteins - metabolism ; Rats ; Rats, Sprague-Dawley ; Transcription, Genetic - drug effects ; Transfection ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2000-09, Vol.279 (3), p.H939-H945</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-df978295c9492ddca2546933cca30396096d27de3bc49326f5987ef9e613a3713</citedby><cites>FETCH-LOGICAL-c401t-df978295c9492ddca2546933cca30396096d27de3bc49326f5987ef9e613a3713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10993753$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mustapha, Shareef</creatorcontrib><creatorcontrib>Kirshner, Alla</creatorcontrib><creatorcontrib>De Moissac, Danielle</creatorcontrib><creatorcontrib>Kirshenbaum, Lorrie A</creatorcontrib><title>A direct requirement of nuclear factor-kappa B for suppression of apoptosis in ventricular myocytes</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Faculty of Medicine, Department of Physiology, Institute of
Cardiovascular Sciences, St. Boniface General Hospital Research Centre,
University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6
Nuclear factor- B
(NF- B) is a ubiquitously expressed cellular factor regulated by the
cytoplasmic factor inhibitor protein B (I B ). Activation of
NF- B by cytokines, including tumor necrosis factor- (TNF- ),
requires the phosphorylation and degradation of I B . An
anti-apoptotic role for NF- B has recently been suggested. In
the present study, we ascertained whether death-promoting signals and
apoptosis mediated by TNF- are suppressed by NF- B in postnatal ventricular myocytes. Stimulation of myocytes with TNF- resulted in
a 12.1-fold increase ( P < 0.01) in NF- B-dependent
gene transcription and DNA binding compared with controls. This was
accompanied by a corresponding increase in the NF- B target protein
A20 as determined by Western blot analysis. Vital staining revealed
that TNF- was not cytotoxic to myocytes and did not provoke
apoptosis. Adenovirus-mediated delivery of a nonphosphorylatable form
of I B to inactivate NF- B prevented TNF- -stimulated
NF- B-dependent gene transcription and nuclear NF- B DNA binding.
Importantly, myocytes stimulated with TNF- and defective for NF- B
activation resulted in a 2.2-fold increase ( P < 0.001)
in apoptosis. To our knowledge, the data provide the first indication
that a functional NF- B signaling pathway is crucial for suppressing
death-promoting signals mediated by TNF- in ventricular myocytes.
adenovirus; inflammation; cytokines; heart failure</description><subject>Adenoviridae - genetics</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Cell Count - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Ceramides - pharmacology</subject><subject>Coloring Agents</subject><subject>DNA Fragmentation - drug effects</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Genes, Reporter - genetics</subject><subject>Heart Ventricles - cytology</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - metabolism</subject><subject>I-kappa B Proteins</subject><subject>Mutagenesis, Site-Directed</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>NF-kappa B - pharmacology</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>Proteins - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transfection</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kF1PwyAUhonRuDn9C4Y_0AqctR3eTeOcyRJv5jVhFLbObiC0av-9NPNjN15xEt7nPTkPQpiSlNKM3cit22jpm5QRQlJW8BTSOQd-gobxmyU0A36KhgRySHIK2QBdhLCN2azI4RwNKOEcigyGSE1xWXmtGuz1Wxunnd432Bq8b1UdV2AjVWN98iqdk_gOG-txaJ3zOoTK7vukdNY1NlQBV3v8HnFfqbaO6K6zqmt0uERnRtZBX32_I_Qye1jez5PF8-PT_XSRqDGhTVIaXkwYzxQfc1aWSrJsnHMApSQQ4DnhecmKUsNKjTmw3GR8UmjDdbxQQkFhhCaHXuVtCF4b4Xy1k74TlIjem_jxJnpvInoTIHpvEb0-oK5d7XR5BB5ExUB6CGyq9eYjehJu00UDtV13R7XHjbf_A7O2rpf6s_kl_0DhSgNfCruTwQ</recordid><startdate>20000901</startdate><enddate>20000901</enddate><creator>Mustapha, Shareef</creator><creator>Kirshner, Alla</creator><creator>De Moissac, Danielle</creator><creator>Kirshenbaum, Lorrie A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20000901</creationdate><title>A direct requirement of nuclear factor-kappa B for suppression of apoptosis in ventricular myocytes</title><author>Mustapha, Shareef ; Kirshner, Alla ; De Moissac, Danielle ; Kirshenbaum, Lorrie A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-df978295c9492ddca2546933cca30396096d27de3bc49326f5987ef9e613a3713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenoviridae - genetics</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Cell Count - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Ceramides - pharmacology</topic><topic>Coloring Agents</topic><topic>DNA Fragmentation - drug effects</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Genes, Reporter - genetics</topic><topic>Heart Ventricles - cytology</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - metabolism</topic><topic>I-kappa B Proteins</topic><topic>Mutagenesis, Site-Directed</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NF-kappa B - pharmacology</topic><topic>NF-KappaB Inhibitor alpha</topic><topic>Proteins - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Transcription, Genetic - drug effects</topic><topic>Transfection</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mustapha, Shareef</creatorcontrib><creatorcontrib>Kirshner, Alla</creatorcontrib><creatorcontrib>De Moissac, Danielle</creatorcontrib><creatorcontrib>Kirshenbaum, Lorrie A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mustapha, Shareef</au><au>Kirshner, Alla</au><au>De Moissac, Danielle</au><au>Kirshenbaum, Lorrie A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A direct requirement of nuclear factor-kappa B for suppression of apoptosis in ventricular myocytes</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2000-09-01</date><risdate>2000</risdate><volume>279</volume><issue>3</issue><spage>H939</spage><epage>H945</epage><pages>H939-H945</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Faculty of Medicine, Department of Physiology, Institute of
Cardiovascular Sciences, St. Boniface General Hospital Research Centre,
University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6
Nuclear factor- B
(NF- B) is a ubiquitously expressed cellular factor regulated by the
cytoplasmic factor inhibitor protein B (I B ). Activation of
NF- B by cytokines, including tumor necrosis factor- (TNF- ),
requires the phosphorylation and degradation of I B . An
anti-apoptotic role for NF- B has recently been suggested. In
the present study, we ascertained whether death-promoting signals and
apoptosis mediated by TNF- are suppressed by NF- B in postnatal ventricular myocytes. Stimulation of myocytes with TNF- resulted in
a 12.1-fold increase ( P < 0.01) in NF- B-dependent
gene transcription and DNA binding compared with controls. This was
accompanied by a corresponding increase in the NF- B target protein
A20 as determined by Western blot analysis. Vital staining revealed
that TNF- was not cytotoxic to myocytes and did not provoke
apoptosis. Adenovirus-mediated delivery of a nonphosphorylatable form
of I B to inactivate NF- B prevented TNF- -stimulated
NF- B-dependent gene transcription and nuclear NF- B DNA binding.
Importantly, myocytes stimulated with TNF- and defective for NF- B
activation resulted in a 2.2-fold increase ( P < 0.001)
in apoptosis. To our knowledge, the data provide the first indication
that a functional NF- B signaling pathway is crucial for suppressing
death-promoting signals mediated by TNF- in ventricular myocytes.
adenovirus; inflammation; cytokines; heart failure</abstract><cop>United States</cop><pmid>10993753</pmid><doi>10.1152/ajpheart.2000.279.3.H939</doi></addata></record> |
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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2000-09, Vol.279 (3), p.H939-H945 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_279_3_H939 |
| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adenoviridae - genetics Animals Apoptosis - drug effects Cell Count - drug effects Cell Survival - drug effects Cells, Cultured Ceramides - pharmacology Coloring Agents DNA Fragmentation - drug effects DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Genes, Reporter - genetics Heart Ventricles - cytology Heart Ventricles - drug effects Heart Ventricles - metabolism I-kappa B Proteins Mutagenesis, Site-Directed Myocardium - cytology Myocardium - metabolism NF-kappa B - metabolism NF-kappa B - pharmacology NF-KappaB Inhibitor alpha Proteins - metabolism Rats Rats, Sprague-Dawley Transcription, Genetic - drug effects Transfection Tumor Necrosis Factor-alpha - pharmacology |
| title | A direct requirement of nuclear factor-kappa B for suppression of apoptosis in ventricular myocytes |
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