Page 64 - F. Cell biology

[F. Cell biology-40]

Arachidonic acid metabolite, 17(18)-epoxyeicosatetraenoic

acid, attenuates profibrotic signalling in idiopathic

pulmonary fibrosis

Sujin Moon¹, Miae Kim¹, Gi Won Hwang¹, Hyun Ju Yoo², Jin Woo Song¹˙*

¹Department of Pulmonary and Critical Care Medicine, Asan Medical Institute of Convergence Science and

Technology, Asan Medical Center, University of Uls, Seoul 05505, Republic of Korea, ²Convergence Medicine, Asan
Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Uls, Seoul 05505,

Republic of Korea

Background: Arachidonic acid metabolite,17(18)-Epoxyeicosatetraenoic acid (EpETE) is a lipid metabolite from dietary
omega-3 polyunsaturated fatty acids such as eicosapentaenoic acid (EPA). 17(18)-EpETE is known to have anti-

inflammatory effect but its effect on pulmonary fibrosis remain to be investigated.

Methods: EPETEs were analyzed with Agilent 7890/5975 GC/MSD system and HP-5 MS column in the human lung

tissues (IPF and controls). The role of 17(18)-EpETE was evaluated using in vitro pulmonary fibrosis models. The
levels of protein or mRNA in cell lysates was measured by western blot assays or RT-qPCR

Results: The level of 17(18)-EpETE was significantly reduced in lung tissues from IPF patients compared with that in
controls. 17(18)-EpETE reduced the TGF-β1- induced protein expression of fibrotic markers in lung fibroblast. Also,

17(18)-EpETE reduced the TGF-β1-induced protein expression of epithelial mesenchymal transition (EMT)-related
genes (fibronectin) in Beas-2B cells. Moreover, 17(18)-EpETE reduced mRNA levels of TGF-β1-induced EMT-related

genes (SNAIL, SLUG) in Beas-2B cells.

Conclusions: Our results suggest that 17(18)-EpETE may have anti-fibrotic effects on pulmonary fibrosis by

suppressing activation of fibroblasts and EMT of epithelial cells.