Comparative transcriptomic analysis of mice liver treated with different AMPK activators in a mice model of atherosclerosis
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Ang Ma1,2,*, Dongmei Wang1,*, Yuanyuan An1, Wei Fang3, Haibo Zhu1
1State Key Laboratory for Bioactive Substances and Functions of Natural Medicines, Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, China
2Department of Basic Medical Sciences, Medical College, Xiamen University, Xiamen, China
3Department of Nuclear Medicine, Fu Wai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, China
*These authors contributed equally to this work and should be considered co-first authors
Haibo Zhu, email: email@example.com
Wei Fang, email: firstname.lastname@example.org
Keywords: AMPK activators, atherosclerosis, IMM-H007, A-769662, metformin
Received: November 22, 2016 Accepted: January 24, 2017 Published: February 02, 2017
Atherosclerosis is known to be the primary underlying factor responsible for the development of cardiovascular diseases. Suppression of AMP-activated protein kinase stimulates arterial deposition of excess lipids, resulting in the development of atherosclerotic lesions. In this study we successfully developed the disease model of mice and mimicked the therapeutic effect, for that we chose three different AMP-activated protein kinase activators (IMM-H007, A-769662 and Metformin) to identify which one has a superior effect in the atherosclerosis model. We combined the transcriptomes of four groups of mice liver including high-fat diet group and the experimental groups treated with different AMP-activated protein kinase activators. We analyzed the increased genes to candidate metabolic and disease pathways. Compared to the high-fat diet group, a total of 799 differentially expressed genes were identified in treatment groups. There were 291, 473, and 323 differentially expressed genes in H007, Metformin, and A-769662 group respectively. And seven statistically significant pathways were observed in both H007 and Metformin groups. We expect that gene expression profiling in the mice model would extend our understanding of atherosclerosis in the molecular level. This study provides a fundamental framework for future clinical research on human atherosclerosis and new clues for developing novel drugs for the treatment of atherosclerosis.
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