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Identification of Proteins Responding to Adrenergic Receptor Subtype-Specific Hypertrophy in Cardiomyocytes by Proteomic Approaches

Ning Liu1*#, Kai-zheng Gong2,3#, Yuan-bin Cai2, and Zijian Li2*

1Central Laboratory, Jilin University Second Hospital, Changchun 130041, P.R. China; fax: +86 (431) 8879-6510; E-mail: liu_ning@jlu.edu.cn

2Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health and Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100091, P.R. China; fax: +86 (10) 6201-7700; E-mail: lizijian@bjmu.edu.cn; caiyuanbin@bjmu.edu.cn

3Department of Cardiology, The First People’s Hospital of Yangzhou, Yangzhou 225001, P.R. China; E-mail: yungkzh@163.com

* To whom correspondence should be addressed.

# These authors contributed equally to this work.

Received December 17, 2010; Revision received April 25, 2011
The individual signaling pathways underlying cardiac hypertrophy, which is induced by either α or β adrenergic receptor (AR), are different. Activation of different AR subtypes couples to different G proteins and induction of specific signaling pathways, which ultimately results in subtype-specific regulation of cardiac function. We present the first proteomics study identifying proteins that are related to AR subtype-specific hypertrophy in cardiomyocytes by comparing the two-dimensional electrophoresis patterns between neonatal rat cardiomyocytes treated by phenylepinephrin (PE) and by isoproterenol (ISO). An improved 2-DE strategy was used in these comparative experiments. Twenty-five differentially expressed proteins in cardiomyocytes treated by PE or treated by ISO were successfully analyzed and identified using matrix-assisted laser desorption/ionization-time of flight mass spectrometry, especially those that might be responsible to intracellular oxidative stress such as dismutase, peroxiredoxin, and thioredoxin-like protein p46. In addition, induced reactive oxygen species were also found to be AR subtype-specifically relevant to endoplasmic reticulum proteinase ERK1/2 phosphorylation during the development of hypertrophy induced by different AR subtypes. The results will help to better understand the underlying mechanisms of different adrenergic receptor subtype-induced hypertrophy.
KEY WORDS: adrenergic receptors, cardiac hypertrophy, proteomics, reactive oxygen species

DOI: 10.1134/S0006297911100075