| First Author | Sharma N | Year | 2012 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 32 |
| Issue | 12 | Pages | 2836-8 |
| PubMed ID | 23065827 | Mgi Jnum | J:208312 |
| Mgi Id | MGI:5562632 | Doi | 10.1161/ATVBAHA.112.300471 |
| Citation | Sharma N, et al. (2012) Myeloid Kruppel-like factor 4 deficiency augments atherogenesis in ApoE-/- mice--brief report. Arterioscler Thromb Vasc Biol 32(12):2836-8 |
| abstractText | OBJECTIVE: To investigate the role of Kruppel-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. |
