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• W2168144830 abstract "Cystic fibrosis (CF) remains a fatal progressive disease in spite of the discovery and characterization of the CFTR gene. Transforming growth factor beta (TGF-beta) has been implicated in pathophysiology of CF. Previous reports have shown the trans-Golgi network (TGN) is hyperacdified in CF epithelial cells in culture and that this hyperacidification can be corrected with the membrane permeant weak base, chloroquine. In this study bioactive TGF-beta produced by CF and normal cells was measured using a reporter cell line with a TGF-beta responsive promoter linked to luciferase. Increased levels of TGF-beta were detected in the conditioned media from CF epithelial cells compared to their matched controls-(IB3-1 vs. S9; pCEP-R vs. pCEP, CuFi-4 vs. NuLi-1). Levels of TGF-beta were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-beta levels." @default.
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• W2168144830 date "2006-01-01" @default.
• W2168144830 modified "2023-09-24" @default.
• W2168144830 title "Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells" @default.
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• W2168144830 doi "https://doi.org/10.1002/ppul.20452" @default.
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