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The Scientific World Journal
Volume 2012 (2012), Article ID 248320, 8 pages
Research Article

Activation of β-Adrenoceptors by Dobutamine May Induce a Higher Expression of Peroxisome Proliferator-Activated Receptors δ (PPARδ) in Neonatal Rat Cardiomyocytes

1Department of Cardiology and Department of Medical Research, Chi-Mei Medical Center, Yong Kang, Tainan 73101, Taiwan
2Department of Cardiology and Internal Medicine, Taipei City Hospital-Zhongxing Branch, Taipei 10341, Taiwan
3Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
4Graduate Institute of Basic Medical Science, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan
5Institute of Medical Sciences, Chang Jung Christian University, Quei-Ren, Tainan 71101, Taiwan

Received 19 January 2012; Accepted 28 February 2012

Academic Editor: Syu-ichi Hirai

Copyright © 2012 Ming-Ting Chou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Recent evidence showed the role of peroxisome proliferator-activated receptors (PPARs) in cardiac function. Cardiac contraction induced by various agents is critical in restoring the activity of peroxisome proliferator-activated receptors δ (PPARδ) in cardiac myopathy. Because dobutamine is an agent widely used to treat heart failure in emergency setting, this study is aimed to investigate the change of PPARδ in response to dobutamine. Neonatal rat cardiomyocytes were used to examine the effects of dobutamine on PPARδ expression levels and cardiac troponin I (cTnI) phosphorylation via Western blotting analysis. We show that treatment with dobutamine increased PPARδ expression and cTnI phosphorylation in a time- and dose-dependent manner in neonatal rat cardiomyocytes. These increases were blocked by the antagonist of β1-adrenoceptors. Also, the action of dobutamine was related to the increase of calcium ions and diminished by chelating intracellular calcium. Additionally, dobutamine-induced action was reduced by the inhibition of downstream messengers involved in this calcium-related pathway. Moreover, deletion of PPARδ using siRNA generated the reduction of cTnI phosphorylation in cardiomyocytes treated with dobutamine. Thus, we concluded that PPARδ is increased by dobutamine in cardiac cells.