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CircRNA-012091/PPP1R13B-mediated lung fibrotic response in silicosis via endoplasmic reticulum stress and autophagy
Abstract
Abstract Silicosis is a progressive fibrotic disease of lung tissue caused by long-term inhalation of SiO2. However, relatively few studies of the direct effects of SiO2 on lung fibroblasts have been performed. PPP1R13B is a major member of the apoptosis-stimulating proteins of the p53 family, but its role in pulmonary fibrosis is unclear. To elucidate the role of PPP1R13B in the pathological process of silicosis, we explored the molecular mechanisms related to PPP1R13B and the functional effects of proliferation and migration of fibroblasts. Through lentivirus transfection, Western blotting, and fluorescent in situ hybridization experiments, we found that SiO2 downregulated circRNA-012091 (circ-012091) expression in lung fibroblasts and induced upregulation of downstream PPP1R13B. Transfection of L929 cells with PPP1R13B CRISPR NIC plasmid inhibited the upregulation of endoplasmic reticulum stress (ERS) and autophagy-related protein expression in lung fibroblasts treated with SiO2, and induced decreases in cell proliferation, migration, and viability. Transfection of L929 cells with the PPP1R13B CRISPR ACT plasmid induced increases in cell proliferation, migration, and viability. In addition, the ERS inhibitor salubrinal and the autophagy inhibitor 3-methyladenine inhibited the increased migration of L929 cells transfected with the PPP1R13B CRISPR ACT plasmid. These results suggest that PPP1R13B regulated by circ-012091 promotes the proliferation and migration of lung fibroblasts through ERS and autophagy, and plays a crucial role in the development of pulmonary fibrosis in silicosis.
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PPP1R13B regulated by mmu_circ_012091 contributes to the proliferation and migration of lung fibroblasts that rely on endoplasmic reticulum stress (ERS) and autophagy.
“According to recent research, protein phosphatase 1 regulatory subunit 13B (PPP1R13B) regulated by mmu_circ_012091 contributes to the proliferation and migration of lung fibroblasts that rely on endoplasmic reticulum stress (ERS) and autophagy [107].”
From Circular RNAs in depression: Biogenesis, function, expression, and therapeutic potential (2021) · cites this paper as [107]
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Metadata
- Authors
- Cheng, Y., Luo, W., Li, Z., Cao, M., Zhu, Z., Han, C., Dai, X., Zhang, W., Wang, J., Yao, H., & Chao, J.
- Affiliations
- Zhongda Hospital Southeast University (CN)
- Department of Physiology
- Department of Pharmacology, School of Medicine, and
- Corresponding author
- Chao, Jie
- Venue
- American Journal of Respiratory Cell and Molecular Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-09-01
- Volume
- 61
- Issue
- 3
- Pages
- 380-391
- ISSN
- 1044-1549 (ISSN-L)
- 1535-4989
- OpenAlex
- W2927056646
- Cited by
- 70
- References
- 48
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 11 · 2023: 4 · 2022: 14 · 2021: 19 · 2020: 11 · 2019: 3
- FWCI
- 8.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Circular RNAs in diseases
- Keywords
- silicosis, pulmonary fibrosis, endoplasmic reticulum stress, autophagy, lung fibroblasts, silica, fibroblast proliferation, cell migration, salubrinal, 3-methyladenine, CRISPR interference
- MeSH terms
- RNA, Circular, Autophagy, Cell Movement, Fibroblasts, Humans, Lung, Pulmonary Fibrosis, Silicon Dioxide, Signal Transduction, Apoptosis, In Situ Hybridization, Fluorescence, Cell Proliferation, Apoptosis Regulatory Proteins, Endoplasmic Reticulum Stress
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