Myeloid Krüppel-like factor 4 deficiency augments atherogenesis in ApoE-/- mice--brief report.
Arterioscler Thromb Vasc Biol
; 32(12): 2836-8, 2012 Dec.
Article
in En
| MEDLINE
| ID: mdl-23065827
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 ANDRESULTS:
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:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Apolipoproteins E
/
Atherosclerosis
/
Kruppel-Like Transcription Factors
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Arterioscler Thromb Vasc Biol
Journal subject:
ANGIOLOGIA
Year:
2012
Type:
Article
Affiliation country:
United States