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

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Park S,Kim S,Kim MJ,Hong Y,Lee AY,Lee H,Tran Q,Kim M,Cho H,Park J,Kim KP,Park J,Cho MH

doi

10.1016/j.bbrc.2017.11.049

subject

Has Abstract

pub_date

2018-01-01 00:00:00

pages

594-600

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(17)32227-1

journal_volume

495

pub_type

杂志文章

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