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Article: Transient activation of P38 MAP kinase and up-regulation of Pim-1 kinase in cardiac hypertrophy despite no activation of AMPK

TitleTransient activation of P38 MAP kinase and up-regulation of Pim-1 kinase in cardiac hypertrophy despite no activation of AMPK
Authors
Issue Date2008
Citation
Journal of Molecular and Cellular Cardiology, 2008, v. 45 n. 3, p. 404-410 How to Cite?
AbstractAMP-activated protein kinase (AMPK), is an important regulator of cardiac metabolism, but its role is not clearly understood in pressure overload induced hypertrophy. In addition, the relationship between AMPK and other important protein kinases such as p38 MAP kinase, Akt and Pim-1 is unclear. Thus we studied the time course of AMPK activity and phosphorylation of Thr-172 of its α-subunit during the development of cardiac hypertrophy. In parallel, we examined the expression and activation of key kinases known to be involved in cardiac hypertrophy that could interact with AMPK (i.e. p38 MAP kinase, Akt and Pim-1). Male C57BL/6J mice underwent sham or transverse aortic constriction (TAC) surgery and the hearts were harvested 2, 4, 6 and 8 weeks later. Despite significant left ventricular (LV) hypertrophy, LV dilation and impaired LV contractile function at all time points in TAC compared to sham mice, the activity and phosphorylation of AMPK were similar to sham. In contrast, p38 and Pim-1 protein expression was transiently increased in TAC mice at 2 and 4 weeks and at 2, 4 and 6 weeks, respectively. In addition, p38 activation by phosphorylation was also transiently increased at 2 to 6 weeks. There were no differences between sham and TAC mice in p38, Akt or Pim-1 at 8 weeks. In conclusion, TAC resulted in a transient up-regulation in the expression of p38 and Pim-1 despite no activation of AMPK or Akt. © 2008 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/195865
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLei, B-
dc.contributor.authorChess, DJ-
dc.contributor.authorKeung, W-
dc.contributor.authorO'Shea, KM-
dc.contributor.authorLopaschuk, GD-
dc.contributor.authorStanley, WC-
dc.date.accessioned2014-03-19T01:46:11Z-
dc.date.available2014-03-19T01:46:11Z-
dc.date.issued2008-
dc.identifier.citationJournal of Molecular and Cellular Cardiology, 2008, v. 45 n. 3, p. 404-410-
dc.identifier.issn0022-2828-
dc.identifier.urihttp://hdl.handle.net/10722/195865-
dc.description.abstractAMP-activated protein kinase (AMPK), is an important regulator of cardiac metabolism, but its role is not clearly understood in pressure overload induced hypertrophy. In addition, the relationship between AMPK and other important protein kinases such as p38 MAP kinase, Akt and Pim-1 is unclear. Thus we studied the time course of AMPK activity and phosphorylation of Thr-172 of its α-subunit during the development of cardiac hypertrophy. In parallel, we examined the expression and activation of key kinases known to be involved in cardiac hypertrophy that could interact with AMPK (i.e. p38 MAP kinase, Akt and Pim-1). Male C57BL/6J mice underwent sham or transverse aortic constriction (TAC) surgery and the hearts were harvested 2, 4, 6 and 8 weeks later. Despite significant left ventricular (LV) hypertrophy, LV dilation and impaired LV contractile function at all time points in TAC compared to sham mice, the activity and phosphorylation of AMPK were similar to sham. In contrast, p38 and Pim-1 protein expression was transiently increased in TAC mice at 2 and 4 weeks and at 2, 4 and 6 weeks, respectively. In addition, p38 activation by phosphorylation was also transiently increased at 2 to 6 weeks. There were no differences between sham and TAC mice in p38, Akt or Pim-1 at 8 weeks. In conclusion, TAC resulted in a transient up-regulation in the expression of p38 and Pim-1 despite no activation of AMPK or Akt. © 2008 Elsevier Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofJournal of Molecular and Cellular Cardiology-
dc.titleTransient activation of P38 MAP kinase and up-regulation of Pim-1 kinase in cardiac hypertrophy despite no activation of AMPK-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yjmcc.2008.06.008-
dc.identifier.pmid18639556-
dc.identifier.scopuseid_2-s2.0-50849099136-
dc.identifier.volume45-
dc.identifier.issue3-
dc.identifier.spage404-
dc.identifier.epage410-
dc.identifier.isiWOS:000259266200008-

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