2. Academic Validation
  3. LGALS3 regulates endothelial-to-mesenchymal transition via PI3K/AKT signaling pathway in silica-induced pulmonary fibrosis

LGALS3 regulates endothelial-to-mesenchymal transition via PI3K/AKT signaling pathway in silica-induced pulmonary fibrosis

  • Toxicology. 2024 Dec:509:153962. doi: 10.1016/j.tox.2024.153962.
Demin Cheng 1,  Wenxiu Lian 2,  Xinying Jia 2,  Ting Wang 3,  Wenqing Sun 2,  Yi Liu 4,  Chunhui Ni 5
Affiliations

Affiliations

  • 1 Department of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China; Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China.
  • 2 Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China.
  • 3 Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Department of Pathology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210000, China.
  • 4 Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China. Electronic address: liuyinjmu@163.com.
  • 5 Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Department of Public Health, Kangda College of Nanjing Medical University, Lianyungang 320700, China. Electronic address: chninjmu@126.com.
PMID: 39353502 DOI: 10.1016/j.tox.2024.153962
Abstract

Silicosis is a progressive and chronic occupational lung disease characterized by lung inflammation, silicotic nodule formation, and diffuse pulmonary fibrosis. Emerging evidence indicates that endothelial-mesenchymal transition (EndoMT) plays a crucial role in the development of silicosis. Herein, we conducted a SiO2-induced EndoMT model and established a mouse model with pulmonary fibrosis by silica. We identified that SiO2 effectively increased the expression of mesenchymal markers while decreasing the levels of endothelial markers in endothelial cells. It's further demonstrated that SiO2 induced the PI3K/Akt signaling pathway activation via LGALS3 synthesis. Next, interfering LGALS3 blocked the process of EndoMT by inhibiting the activity of PI3K/Akt signaling. In vivo, the administration of a specific PI3K Inhibitor LY294002 significantly alleviated silica-induced pulmonary fibrosis. Collectively, these results identified that the LGALS3/PI3K/Akt pathway provided a rationale target for the clinical treatment and intervention of silicosis.

Keywords

EndoMT; LGALS3; PI3K/AKT; Silicosis.

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