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Sci China Life Sci. 2022 Jan;65(1):193-205. doi: 10.1007/s11427-020-1875-x. Epub 2021 Mar 16.

GM130 regulates pulmonary surfactant protein secretion in alveolar type II cells.

Science China. Life sciences

Qianqian Pang, Chunyi Liu, Yulong Qiao, Jian Zhao, Sin Man Lam, Mei Mei, Guanghou Shui, Shilai Bao, Qiuling Li

Affiliations

  1. State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, The Innovative Academy of Seed Design, Chinese Academy of Sciences, Beijing, 100101, China.
  2. Institute of Forensic Medicine and Laboratory Medicine, Jining Medical University, Jining, 272067, China.
  3. Department of Health Sciences, Institute of Physical Science and Information Technology, Anhui University, Hefei, 230601, China.
  4. State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, The Innovative Academy of Seed Design, Chinese Academy of Sciences, Beijing, 100101, China. [email protected].
  5. School of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China. [email protected].
  6. Department of Health Sciences, Institute of Physical Science and Information Technology, Anhui University, Hefei, 230601, China. [email protected].

PMID: 33740186 DOI: 10.1007/s11427-020-1875-x

Abstract

Pulmonary surfactant is a lipid-protein complex secreted by alveolar type II epithelial cells and is essential for the maintenance of the delicate structure of mammalian alveoli to promote efficient gas exchange across the air-liquid barrier. The Golgi apparatus plays an important role in pulmonary surfactant modification and secretory trafficking. However, the physiological function of the Golgi apparatus in the transport of pulmonary surfactants is unclear. In the present study, deletion of GM130, which encodes for a matrix protein of the cis-Golgi cisternae, was shown to induce the disruption of the Golgi structure leading to impaired secretion of lung surfactant proteins and lipids. Specifically, the results of in vitro and in vivo analysis indicated that the loss of GM130 resulted in trapping of Sftpa in the endoplasmic reticulum, Sftpb and Sftpc accumulation in the Golgi apparatus, and an increase in the compensatory secretion of Sftpd. Moreover, global and epithelial-specific GM130 knockout in mice resulted in an enlargement of alveolar airspace and an increase in alveolar epithelial autophagy; however, surfactant repletion partially rescued the enlarged airspace defects in GM130-deficient mice. Therefore, our results demonstrate that GM130 and the mammalian Golgi apparatus play a critical role in the control of surfactant protein secretion in pulmonary epithelial cells.

© 2021. Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature.

Keywords: Alveolar type II cells; GM130; Golgi apparatus; surfactant protein

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