This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Homeister, J. W. Articles by Patterson, C. Search for Related Content PubMed PubMed Citation Articles by Homeister, J. W. Articles by Patterson, C. Related Collections Related Article

(Circulation Research. 2008;103:687.)
© 2008 American Heart Association, Inc.

Editorials

Zinc Fingers in the Pizza Pie Aorta

Jonathon W. Homeister, Cam Patterson

From the Carolina Cardiovascular Biology Center, Departments of Pathology (J.W.H.) and Medicine (C.P.), School of Medicine, University of North Carolina at Chapel Hill.

Correspondence to Cam Patterson, MD, Director, Division of Cardiology and Carolina Cardiovascular Biology Center, University of North Carolina, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599-7126. E-mail cpatters@med.unc.edu

See related article, pages 690–693

Key Words: macrophages • endothelial cells • transcription factors

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The multifactorial etiology of atherosclerosis includes inflammatory and immune processes that involve numerous cell types, including monocytic and lymphocytic leukocytes, endothelial cells, smooth muscle cells, and fibroblasts. It is likely that each of these cell types, as a contributor to the atherosclerotic process, possesses a gene expression profile unique to its role in disease pathogenesis, although perhaps also dependent on the disease stage, as well as on genetic and environmental factors. Modulation of gene expression patterns by various transcription factors will therefore dictate how a particular cell type contributes to the atherosclerotic process. Krüppel-like factors (KLFs) are a subclass of zinc finger transcription factors originally implicated in cell growth and differentiation. KLF2 and KLF4 in particular regulate the expression of certain genes relevant to atherosclerosis in a shear-dependent manner in endothelial cells and monocytes.¹ It is therefore important to understand the mechanisms and consequences of KLF activation in these cell types in vitro and in vivo. Such studies have the potential to uncover previously unknown transcriptional links between shear-dependent monocytic and endothelial processes that may underlie the pathogenesis of atherosclerosis.

The study by Atkins et al² in the issue of Circulation Research addresses this issue directly using mice with a hemizygous deficiency of KLF2 (KLF2^+/–) and on the ApoE^–/– background to examine the role of KLF2 in atherosclerosis. Aortic lesion extent was increased 30% to 35% in KLF2^+/– mice compared to control littermates. The increase in atherosclerosis in the KLF2^+/– mice was associated with no alterations in aortic expression . . . [Full Text of this Article]

Related Article:

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, and Mukesh K. Jain
Circ. Res. 2008 103: 690-693. [Abstract] [Full Text] [PDF]