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Asian Dust Particles Induce TGF-β(1) via Reactive Oxygen Species in Bronchial Epithelial Cells

BACKGROUND: Asian dust storms can be transported across eastern Asia. In vitro, Asian dust particle-induced inflammation and enhancement of the allergic reaction have been observed. However, the fibrotic effects of Asian dust particles are not clear. Production of transforming growth factor β(1) (TG...

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Detalles Bibliográficos
Autores principales: Kyung, Sun Young, Yoon, Jin Young, Kim, Yu Jin, Lee, Sang Pyo, Park, Jeong-Woong, Jeong, Sung Hwan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Academy of Tuberculosis and Respiratory Diseases 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492378/
https://www.ncbi.nlm.nih.gov/pubmed/23166540
http://dx.doi.org/10.4046/trd.2012.73.2.84
Descripción
Sumario:BACKGROUND: Asian dust storms can be transported across eastern Asia. In vitro, Asian dust particle-induced inflammation and enhancement of the allergic reaction have been observed. However, the fibrotic effects of Asian dust particles are not clear. Production of transforming growth factor β(1) (TGF-β(1)) and fibronectin were investigated in the bronchial epithelial cells after exposure to Asian dust particulate matter (AD-PM10). METHODS: During Asian dust storm periods, air samples were collected. The bronchial epithelial cells were exposed to AD-PM10 with and without the antioxidant, N-acetyl-L-cysteine (NAC). Then TGF-β(1) and fibronectin were detected by Western blotting. The reactive oxygen species (ROS) was detected by the measurement of dicholorodihydrofluorescin (DCF), using a FACScan, and visualized by a confocal microscopy. RESULTS: The expression of TGF-β(1), fibronectin and ROS was high after being exposed to AD-PM10, compared to the control. NAC attenuated both TGF-β(1) and fibronectin expression in the AD-PM10-exposed the bronchial epithelial cells. CONCLUSION: AD-PM10 may have fibrotic potential in the bronchial epithelial cells and the possible mechanism is AD-PM10-induced intracellular ROS.