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OC-STAMP Overexpression Drives Lung Alveolar Epithelial Cell Type II Senescence in Silicosis
Author(s) -
Tian Li,
Xinyu Yang,
Dingjie Xu,
Ziyi Gao,
Yi-bing Gao,
Fuyu Jin,
Yaqian Li,
Shupeng Liu,
Shifeng Li,
Xuemin Gao,
Wenchen Cai,
Na Mao,
Zhongqiu Wei,
Heliang Liu,
Ying Sun,
Yang Fang,
Hong Xu
Publication year - 2021
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2021/4158495
Subject(s) - silicosis , senescence , lung , cell , medicine , pathology , biology , microbiology and biotechnology , biochemistry
Cellular senescence has been considered an important driver of many chronic lung diseases. However, the specific mechanism of cellular senescence in silicosis is still unknown. In the present study, silicotic rats and osteoclast stimulatory transmembrane protein ( Ocstamp ) overexpression of MLE-12 cells were used to explore the mechanism of OC-STAMP in cellular senescence in alveolar epithelial cell type II (AEC2). We found an increasing level of OC-STAMP in AEC2 of silicotic rats. Overexpression of Ocstamp in MLE-12 cells promoted epithelial-mesenchymal transition (EMT), endoplasmic reticulum (ER) stress, and cellular senescence. Myosin heavy chain 9 (MYH9) was a potential interacting protein of OC-STAMP. Knockdown of Ocstamp or Myh9 inhibited cellular senescence in MLE-12 cells transfected with pcmv6- Ocstamp . Treatment with 4-phenylbutyrate (4-PBA) to inhibit ER stress also attenuated cellular senescence in vitro or in vivo . In conclusion, OC-STAMP promotes cellular senescence in AEC2 in silicosis.

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