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Circulation Research. 2008;103:690-693
Published online before print August 28, 2008, doi: 10.1161/CIRCRESAHA.108.184663
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(Circulation Research. 2008;103:690.)
© 2008 American Heart Association, Inc.

Report

Hemizygous Deficiency of Krüppel-Like Factor 2 Augments Experimental Atherosclerosis

G. Brandon Atkins, Yunmei Wang, Ganapati H. Mahabeleshwar, Hong Shi, Huiyun Gao, Daiji Kawanami, Viswanath Natesan, Zhiyong Lin, Daniel I. Simon, Mukesh K. Jain

From the University Hospitals Harrington McLaughlin Heart and Vascular Institute, Cleveland, Ohio; and the Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Correspondence to Mukesh K. Jain MD, Wolstein Research Building, 2103 Cornell Rd, Room 4-537, Cleveland, OH 44106-7290. E-mail mukesh.jain2{at}case.edu

Krüppel-like factor (KLF)2 is a central regulator of endothelial and monocyte/macrophage gene expression and function in vitro. Although the composite effects of KLF2 in these 2 cell types predict that it likely inhibits vascular inflammation, the role of KLF2 in this process in vivo is uncharacterized. In this study, we provide evidence that hemizygous deficiency of KLF2 increased diet-induced atherosclerosis in apolipoprotein E–deficient mice. Our studies highlight an important role for KLF2 in primary macrophage foam cell formation via the potential regulation of the key lipid binding protein adipocyte protein 2/fatty acid–binding protein 4. These novel observations establish that KLF2 is an atheroprotective factor.


Key Words: atherosclerosis • Krüppel-like factor 2 • endothelium • macrophage • adipocyte Protein 2


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