期刊
CIRCULATION RESEARCH
卷 103, 期 7, 页码 690-693出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.108.184663
关键词
atherosclerosis; Kruppel-like factor 2; endothelium; macrophage; adipocyte protein 2
资金
- NHLBI NIH HHS [HL088740, P01 HL048743-160011, R01 HL084154-03, R01 HL086548, HL085816, HL086548, R01 HL075427-05, HL72952, HL75427, P01 HL048743-170011, K01 HL088740, R01 HL072952-05, P01 HL48743, R01 HL084154, HL057506, R01 HL075427, R01 HL076754, R01 HL076754-05, HL084154, P01 HL048743, R01 HL085816, HL76754, R01 HL072952, R37 HL057506, R01 HL086548-03, R01 HL057506] Funding Source: Medline
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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