| First Author | Hasan AU | Year | 2015 |
| Journal | Mol Cell Endocrinol | Volume | 406 |
| Pages | 10-8 | PubMed ID | 25697344 |
| Mgi Jnum | J:222029 | Mgi Id | MGI:5643875 |
| Doi | 10.1016/j.mce.2015.02.012 | Citation | Hasan AU, et al. (2015) Eicosapentaenoic acid upregulates VEGF-A through both GPR120 and PPARgamma mediated pathways in 3T3-L1 adipocytes. Mol Cell Endocrinol 406:10-8 |
| abstractText | 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 gamma (PPARgamma) by GW9662 respectively attenuated the EPA-induced augmentation of VEGF-A release by adipocytes. Furthermore, transfection of GPR120 gene alone and PPARgamma 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 PPARgamma binding to PPAR-response element in VEGF-A promoter region. Thus, by the synchronized activation of a membrane receptor GRP120 and a nuclear receptor PPARgamma, EPA enhances VEGF-A production in adipocytes. |
