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GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver

Cited 14 time in Web of Science Cited 15 time in Scopus
Authors
Park, Sungjin; Kim, Sanghwa; Kim, Min Jung; Hong, Youngeun; Lee, Ah Young; Lee, Hyunji; Tran, Quangdon; Kim, Minhee; Cho, Hyeonjeong; Park, Jisoo; Kim, Kwang Pyo; Park, Jongsun; Cho, Myung-Haing
Issue Date
2018-01
Citation
Biochemical and Biophysical Research Communications, Vol.495 No.1, pp.594-600
Keywords
GOLGA2 knockout miceGolgi disruptionAutophagyLung fibrosisLiver fibrosis
Abstract
Autophagy is a biological recycling process via the self-digestion of organelles, proteins, and lipids for energy-consuming differentiation and homeostasis. The Golgi serves as a donor of the double-membraned phagophore for autophagosome assembly. In addition, recent studies have demonstrated that pulmonary and hepatic fibrosis is accompanied by autophagy. However, the relationships among Golgi function, autophagy, and fibrosis are unclear. Here, we show that the deletion of GOLGA2, encoding a cis-Golgi protein, induces autophagy with Golgi disruption. The induction of autophagy leads to fibrosis along with the reduction of subcellular lipid storage (lipid droplets and lamellar bodies) by autophagy in the lung and liver. GOLGA2 knockout mice clearly demonstrated fibrosis features such as autophagy-activated cells, densely packed hepatocytes, increase of alveolar macrophages, and decrease of alveolar surfactant lipids (dipalmitoylphosphatidylcholine). Therefore, we confirmed the associations among Golgi function, fibrosis, and autophagy. Moreover, GOLGA2 knockout mice may be a potentially valuable animal model for studying autophagy-induced fibrosis. (C) 2017 Elsevier Inc. All rights reserved.
ISSN
0006-291X
URI
https://hdl.handle.net/10371/172323
DOI
https://doi.org/10.1016/j.bbrc.2017.11.049
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College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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