GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver |
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Authors: | Sungjin Park Sanghwa Kim Min Jung Kim Youngeun Hong Ah Young Lee Hyunji Lee Quangdon Tran Minhee Kim Hyeonjeong Cho Jisoo Park Kwang Pyo Kim Jongsun Park Myung-Haing Cho |
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Affiliation: | 1. Department of Pharmacology and Medical Science, Metabolic Syndrome and Cell Signaling Laboratory, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea;2. Laboratory of Toxicology, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea;3. Department of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin 17104, Republic of Korea;4. Division of Basic Radiation Bioscience, Korea Institute of Radiological & Medical Science, Seoul, Republic of Korea;5. Graduate School of Convergence Science and Technology, Seoul National University, Suwon 16229, Republic of Korea;6. Graduate Group of Tumor Biology, Seoul National University, Seoul 08826, Republic of Korea;g. Advanced Institute of Convergence Technology, Seoul National University, Suwon 16229, Republic of Korea;h. Institute of GreenBio Science Technology, Seoul National University, Pyeongchang 25354, Republic of Korea |
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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. |
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Keywords: | Golgi disruption Autophagy Lung fibrosis Liver fibrosis |
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