دورية أكاديمية

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

التفاصيل البيبلوغرافية
العنوان: Transient activation of P38 MAP kinase and up-regulation of Pim-1 kinase in cardiac hypertrophy despite no activation of AMPK
المؤلفون: Lopaschuk, GD, Lei, B, Chess, DJ, Keung, W, O'Shea, KM, Stanley, WC
سنة النشر: 2008
المجموعة: University of Hong Kong: HKU Scholars Hub
الوصف: AMP-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. ; link_to_subscribed_fulltext
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 0022-2828
العلاقة: Journal of Molecular and Cellular Cardiology; Journal of Molecular and Cellular Cardiology, 2008, v. 45 n. 3, p. 404-410; 410; WOS:000259266200008; eid_2-s2.0-50849099136; 404; http://hdl.handle.net/10722/195865Test; 45
DOI: 10.1016/j.yjmcc.2008.06.008
الإتاحة: https://doi.org/10.1016/j.yjmcc.2008.06.008Test
http://hdl.handle.net/10722/195865Test
رقم الانضمام: edsbas.57538E3C
قاعدة البيانات: BASE
الوصف
تدمد:00222828
DOI:10.1016/j.yjmcc.2008.06.008