Myeloid Krüppel-like factor 4 deficiency augments atherogenesis in ApoE-/- mice--brief report.
Journal Article
OBJECTIVE: To investigate the role of Krüppel-like factor 4 (KLF4), an essential transcriptional regulator of macrophage polarization (M1/M2), in the pathogenesis of atherosclerosis. METHODS AND RESULTS: Despite the acknowledged importance of macrophages in atherosclerosis, the role of M1 (classically activated or proinflammatory) versus M2 (alternatively activated or anti-inflammatory) macrophages in this process remains incompletely understood. We recently identified KLF4 as a regulator of macrophage subset specification; that is, KLF4 promotes M2 and inhibits M1 phenotype. Here, we provide evidence that KLF4-deficient macrophages exhibit enhanced proinflammatory activation and foam cell formation in response to oxidized lipids. In vivo, myeloid KLF4-deficient mice (ApoE(-/-) background) develop significantly more vascular inflammation and atherosclerotic lesion formation. CONCLUSIONS: Our findings identify myeloid KLF4 as an essential regulator of vascular inflammation and experimental atherogenesis.
Full Text
Duke Authors
Cited Authors
- Sharma, N; Lu, Y; Zhou, G; Liao, X; Kapil, P; Anand, P; Mahabeleshwar, GH; Stamler, JS; Jain, MK
Published Date
- December 2012
Published In
Volume / Issue
- 32 / 12
Start / End Page
- 2836 - 2838
PubMed ID
- 23065827
Pubmed Central ID
- 23065827
Electronic International Standard Serial Number (EISSN)
- 1524-4636
Digital Object Identifier (DOI)
- 10.1161/ATVBAHA.112.300471
Language
- eng
Conference Location
- United States