File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Deficiency of the Bax gene attenuates denervation-induced apoptosis

TitleDeficiency of the Bax gene attenuates denervation-induced apoptosis
Authors
KeywordsBCL-2
Apoptosis
Neuromuscular disease
Muscle atrophy
Issue Date2006
Citation
Apoptosis, 2006, v. 11, n. 6, p. 967-981 How to Cite?
AbstractApoptosis has been implicated in mediating denervation-induced muscle wasting. In this study we determined the effect of interference of apoptosis on muscle wasting during denervation by using mice genetically deficient in pro-apoptotic Bax. After denervation, muscle wasting was evident in both wild-type and Bax -/- muscles but reduction of muscle weight was attenuated in Bax -/- mice. Apoptotic DNA fragmentation increased in wild-type denervated muscles whereas there was no statistical increase in DNA fragmentation in denervated muscles from Bax -/- mice. Mitochondrial AIF and Smac/DIABLO releases and Bcl-2, p53 and HSP27 increased whereas XIAP and MnSOD decreased to a similar extent in muscles from wild-type and Bax -/- mice following denervation. Mitochondrial cytochrome c release was elevated in denervated muscles from wild-type mice but the increase was suppressed in muscles from Bax -/- mice. Increases in caspase-3 and -9 activities and oxidative stress markers H 2 O 2 , MDA/4-HAE and nitrotyrosine were all evident in denervated muscles from wild-type mice but these changes were absent in muscles from Bax -/- mice. Moreover, ARC increased exclusively in denervated Bax -/- muscle. Our data indicate that under conditions of denervation, pro-apoptotic signalling is suppressed and muscle wasting is attenuated when the Bax gene is lacking. These findings suggest that interventions targeting apoptosis may be valuable in ameliorating denervation-associated pathologic muscle wasting in certain neuromuscular disorders that involve partial or full denervation. © 2006 Springer Science + Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/244083
ISSN
2015 Impact Factor: 3.592
2015 SCImago Journal Rankings: 1.554

 

DC FieldValueLanguage
dc.contributor.authorSiu, P. M.-
dc.contributor.authorAlway, S. E.-
dc.date.accessioned2017-08-31T08:56:00Z-
dc.date.available2017-08-31T08:56:00Z-
dc.date.issued2006-
dc.identifier.citationApoptosis, 2006, v. 11, n. 6, p. 967-981-
dc.identifier.issn1360-8185-
dc.identifier.urihttp://hdl.handle.net/10722/244083-
dc.description.abstractApoptosis has been implicated in mediating denervation-induced muscle wasting. In this study we determined the effect of interference of apoptosis on muscle wasting during denervation by using mice genetically deficient in pro-apoptotic Bax. After denervation, muscle wasting was evident in both wild-type and Bax -/- muscles but reduction of muscle weight was attenuated in Bax -/- mice. Apoptotic DNA fragmentation increased in wild-type denervated muscles whereas there was no statistical increase in DNA fragmentation in denervated muscles from Bax -/- mice. Mitochondrial AIF and Smac/DIABLO releases and Bcl-2, p53 and HSP27 increased whereas XIAP and MnSOD decreased to a similar extent in muscles from wild-type and Bax -/- mice following denervation. Mitochondrial cytochrome c release was elevated in denervated muscles from wild-type mice but the increase was suppressed in muscles from Bax -/- mice. Increases in caspase-3 and -9 activities and oxidative stress markers H 2 O 2 , MDA/4-HAE and nitrotyrosine were all evident in denervated muscles from wild-type mice but these changes were absent in muscles from Bax -/- mice. Moreover, ARC increased exclusively in denervated Bax -/- muscle. Our data indicate that under conditions of denervation, pro-apoptotic signalling is suppressed and muscle wasting is attenuated when the Bax gene is lacking. These findings suggest that interventions targeting apoptosis may be valuable in ameliorating denervation-associated pathologic muscle wasting in certain neuromuscular disorders that involve partial or full denervation. © 2006 Springer Science + Business Media, LLC.-
dc.languageeng-
dc.relation.ispartofApoptosis-
dc.subjectBCL-2-
dc.subjectApoptosis-
dc.subjectNeuromuscular disease-
dc.subjectMuscle atrophy-
dc.titleDeficiency of the Bax gene attenuates denervation-induced apoptosis-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10495-006-6315-4-
dc.identifier.pmid16763784-
dc.identifier.scopuseid_2-s2.0-33745018669-
dc.identifier.volume11-
dc.identifier.issue6-
dc.identifier.spage967-
dc.identifier.epage981-
dc.identifier.eissn1573-675X-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats