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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.

OC-STAMP Overexpression Drives Lung Alveolar Epithelial Cell Type II Senescence in Silicosis