转染
血管生成
基因沉默
染色质免疫沉淀
下调和上调
过氧化物酶体增殖物激活受体
血管内皮生长因子
化学
脂肪组织
受体
二十碳五烯酸
生物
分子生物学
内科学
内分泌学
癌症研究
发起人
基因表达
生物化学
脂肪酸
基因
血管内皮生长因子受体
医学
多不饱和脂肪酸
作者
Azeem Hasan,Koji Ohmori,Kuniyoshi Konishi,Jun–ichi Igarashi,Takeshi Hashimoto,Kazuyo Kamitori,Fuminori Yamaguchi,Ikuko Tsukamoto,Toru Uyama,Yasuhiro Ishihara,Takahisa Noma,Masaaki Tokuda,Masakazu Kohno
标识
DOI:10.1016/j.mce.2015.02.012
摘要
Vascular endothelial growth factor-A (VEGF-A) released from adipocytes promotes angiogenesis; and thereby ameliorates the local hypoxia-induced adipose inflammation and insulin resistance. Here, we newly found that eicosapentaenoic acid (EPA) upregulated both mRNA expression and release of VEGF-A in mature 3T3-L1 adipocytes. Silencing mRNA of G-protein coupled receptor 120 (GPR120) and specific inhibition of peroxisome proliferator-activated receptor γ (PPARγ) by GW9662 respectively attenuated the EPA-induced augmentation of VEGF-A release by adipocytes. Furthermore, transfection of GPR120 gene alone and PPARγ gene alone to HEK293 cells respectively increased the promoter activity of VEGF-A as assessed by luciferase reporter assay, which was further augmented when both genes were co-transfected. Promoter deletion analysis and chromatin immunoprecipitation assay revealed that co-transfection of GPR120 enhanced EPA-induced PPARγ binding to PPAR-response element in VEGF-A promoter region. Thus, by the synchronized activation of a membrane receptor GRP120 and a nuclear receptor PPARγ, EPA enhances VEGF-A production in adipocytes.
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