화학공학소재연구정보센터
Biochemical and Biophysical Research Communications, Vol.495, No.3, 2202-2208, 2018
Bromodomain-containing protein 7 deficiency augments atherosclerotic lesions in ApoE(-/-) mice
Atherosclerotic plaque formation is characterized by the persistence of lipid-laden macrophages on the inner walls of arteries. Chronic inflammation and imbalanced macrophage function are likely to play a critical role. Herein, we investigated whether bromodomain-containing protein 7 (Brd7), a member of the bromodomain-containing protein family, regulates atherosclerosis, and if so, which mechanisms are responsible for the process. We found that Brd7 is expressed in mouse atherosclerotic plaques, and mostly in macrophages. Inhibition of Brd7 accelerates atherosclerotic lesion formation in ApoE(-/-) mice by promoting NE-kappa B-mediated inflammation. Furthermore, Brd7 inhibition alters the phenotype of macrophages and promotes plaque instability, at least partly via STAT6 signaling. Our data define a previously undescribed role of Brd7 in the development of atherosclerosis. (C) 2017 Elsevier Inc. All rights reserved.