Oxidized low-density lipoprotein activates adipophilin through ERK1/2 signal pathway in RAW264.7 cells

Authors: Liu, Qingnan; Dai, Zhibing; Liu, Zhiqiang; Liu, Xiaohui; Tang, Chaoke; Wang, Zuo; Yi, Guanghui; Liu, Lushan; Jiang, Zhisheng; Yang, Yongzong; Yuan, Zhonghua

Source: Acta Biochimica et Biophysica Sinica, Volume 42, Number 9, 7 September 2010 , pp. 635-645(11)

Publisher: Oxford University Press

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Abstract:

It has been reported that oxidized low-density lipoprotein (Ox-LDL) can increase the expression of adipophilin. However, the detailed mechanisms are not fully understood. The aim of this study was to investigate the mechanism of Ox-LDL on adipophilin expression and the intracellular lipid droplet accumulation. A mouse macrophage-like cell line, RAW264.7, was used throughout, and it was found that Ox-LDL induced adipophilin expression in a dose-dependent manner. Moreover, Ox-LDL induced peroxisome proliferator-activated receptor- (PPAR) expression and PPAR-specific inhibitor T0070907 abrogated Ox-LDL-induced adipophilin expression, but specific agonist GW1929 not. Furthermore, Ox-LDL induced phosphorylation of ERK1/2, and ERK1/2-specific inhibition by PD98059 suppressed the Ox-LDL-induced PPAR and adipophilin expression. The results showed that ERK1/2 or PPAR-specific inhibition decreased the amounts of intracellular lipid droplets. Meanwhile, the PPAR-specific agonist increased intracellular lipid droplets. These results suggested that Ox-LDL-induced increase in adipophilin level via ERK1/2 activation is one of the mechanisms of inducing greater amounts of intracellular lipid droplets in RAW264.7 cells, which indicated that adipophilin is involved in atherosclerotic progression.

Keywords: adipophilin; ERK1/2; atherosclerosis; PPAR

Document Type: Research article

DOI: http://dx.doi.org/10.1093/abbs/gmq070

Publication date: 2010-09-07