Myeloid Kruppel-like factor 4 deficiency augments atherogenesis in ApoE-/- mice--brief report.

ABSTRACT:

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(-/-

SUBMITTER: Sharma N 

PROVIDER: S-EPMC3574634 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature