Deranged fatty acid composition causes pulmonary fibrosis in Elovl6-deficient mice

Hiroaki Sunaga, Hiroki Matsui, Manabu Ueno, Toshitaka Maeno, Tatsuya Iso, Mas Rizky A. A. Syamsunarno, Saki Anjo, Takashi Matsuzaka, Hitoshi Shimano, Tomoyuki Yokoyama () and Masahiko Kurabayashi
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Hiroaki Sunaga: Gunma University Graduate School of Health Sciences, 3-39-22, Showa-machi, Maebashi 371-8514, Japan
Hiroki Matsui: Gunma University Graduate School of Health Sciences, 3-39-22, Showa-machi, Maebashi 371-8514, Japan
Manabu Ueno: Gunma University Graduate School of Medicine
Toshitaka Maeno: Gunma University Graduate School of Medicine
Tatsuya Iso: Gunma University Graduate School of Medicine
Mas Rizky A. A. Syamsunarno: Gunma University Graduate School of Medicine
Saki Anjo: Gunma University Graduate School of Health Sciences, 3-39-22, Showa-machi, Maebashi 371-8514, Japan
Takashi Matsuzaka: Faculty of Medicine, University of Tsukuba
Hitoshi Shimano: Faculty of Medicine, University of Tsukuba
Tomoyuki Yokoyama: Gunma University Graduate School of Health Sciences, 3-39-22, Showa-machi, Maebashi 371-8514, Japan
Masahiko Kurabayashi: Gunma University Graduate School of Medicine

Nature Communications, 2013, vol. 4, issue 1, 1-14

Abstract: Abstract Despite the established role of alveolar type II epithelial cells for the maintenance of pulmonary function, little is known about the deregulation of lipid composition in the pathogenesis of pulmonary fibrosis. The elongation of long-chain fatty acids family member 6 (Elovl6) is a rate-limiting enzyme catalysing the elongation of saturated and monounsaturated fatty acids. Here we show that Elovl6 expression is significantly downregulated after an intratracheal instillation of bleomycin (BLM) and in human lung with idiopathic pulmonary fibrosis. Elovl6-deficient (Elovl6−/−) mice treated with BLM exhibit severe fibroproliferative response and derangement of fatty acid profile compared with wild-type mice. Furthermore, Elovl6 knockdown induces a change in fatty acid composition similar to that in Elovl6−/− mice, resulting in induction of apoptosis, TGF-β1 expression and reactive oxygen species generation. Our findings demonstrate a previously unappreciated role for Elovl6 in the regulation of lung homeostasis, and in pathogenesis and exacerbation of BLM-induced pulmonary fibrosis.

Date: 2013
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DOI: 10.1038/ncomms3563

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