Oncotarget

Research Papers:

Serum cyclin-dependent kinase 9 is a potential biomarker of atherosclerotic inflammation

Yeming Han, Shanshan Zhao, Yaoqin Gong, Guihua Hou, Xi Li and Li Li _

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Oncotarget. 2016; 7:1854-1862. https://doi.org/10.18632/oncotarget.6443

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Abstract

Yeming Han1, Shanshan Zhao2, Yaoqin Gong2,3, Guihua Hou2, Xi Li2,3,*, Li Li1,*

1Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Department of of Cardiology, Qilu Hospital, Shandong University, Jinan, Shandong, 250012, China

2Laboratory of Experimental Teratology, Ministry of Education, School of Medicine, Shandong University, Jinan, Shandong, 250012, China

3Department of Genetics, School of Medicine, Shandong University, Jinan, Shandong, 250012, China

*These authors contributed equally to this work

Correspondence to:

Li Li, e-mail: lilihospital@163.com

Keywords: atherosclerosis, inflammation, serum, proteomics, CDK9

Received: July 29, 2015     Accepted: November 16, 2015     Published: December 01, 2015

ABSTRACT

Atherosclerotic coronary artery disease (CAD) is one of the most prevalent diseases worldwide. Atherosclerosis was considered to be the single most important contributor to CAD. In this study, a distinct serum protein expression pattern in CAD patients was demonstrated by proteomic analysis with two-dimensional gel electrophoresis coupled with mass spectrometry. In particular, CDK9 was found to be highly elevated in serum, monocytes and artery plaque samples of CAD patients. Furthermore, there was high infiltration of CD14+ monocytes/macrophages within artery plaques correlated with the expression of CDK9. Moreover, Flavopiridol (CDK9 inhibitor) could inhibit THP-1 cell (monocytic acute leukemia cell line) proliferation by targeting CDK9. Altogether, These findings indicate that CDK9 represent an important role for inflammation in the pathogenesis of atherosclerosis. It may be a potential biomarker of atherosclerotic inflammation and offer insights into the pathophysiology and targeted therapy for atherosclerotic CAD.


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