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Publication : Hemizygous deficiency of Krüppel-like factor 2 augments experimental atherosclerosis.

First Author  Atkins GB Year  2008
Journal  Circ Res Volume  103
Issue  7 Pages  690-3
PubMed ID  18757824 Mgi Jnum  J:155153
Mgi Id  MGI:4412355 Doi  10.1161/CIRCRESAHA.108.184663
Citation  Atkins GB, et al. (2008) Hemizygous deficiency of Kruppel-like factor 2 augments experimental atherosclerosis. Circ Res 103(7):690-3
abstractText  Kruppel-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.
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