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Fig. 9 | Particle and Fibre Toxicology

Fig. 9

From: Single-cell transcriptome sequencing–based analysis: probing the mechanisms of glycoprotein NMB regulation of epithelial cells involved in silicosis

Fig. 9

Schematic representation of the mechanism of GPNMB regulation of silica-induced pulmonary fibrosis in alveolar type II epithelial cells. GPNMB expression in AT2 exposed to SiO2 was increased, promoting cell proliferation, accelerating migration, and regulating the EMT process. GPNMB was persistently highly expressed in AT2 and can be released extracellularly with extracellular vesicles to exert its effects, participating in the regulation of phenotypic transformation and functional changes in normal AT2. Fibrotic ECM showed abnormal accumulation of GPNMB, part of which originated from AT2, and GPNMB adhered to ECM in the form of extracellular vesicles to participate in the pulmonary fibrosis process and continued to exert a sustained amplifying effect on ECM accumulation

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Particle and Fibre Toxicology

ISSN: 1743-8977

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