Journal
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
Volume 42, Issue 9, Pages 635-645Publisher
OXFORD UNIV PRESS
DOI: 10.1093/abbs/gmq070
Keywords
adipophilin; ERK1; 2; atherosclerosis; PPAR gamma
Categories
Funding
- National Natural Science Foundation of China [30971268]
- Ministry of Education [(2008)890]
- University of South China [52XQD2200727]
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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-gamma (PPAR gamma) expression and PPAR gamma-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 gamma and adipophilin expression. The results showed that ERK1/2 or PPAR gamma-specific inhibition decreased the amounts of intracellular lipid droplets. Meanwhile, the PPAR gamma-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.
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