Galectin-3 Interacts with the CHI3L1 Axis and Contributes to Hermansky-Pudlak Syndrome Lung Disease

Hermansky-Pudlak syndrome (HPS) comprises a group of inherited disorders caused by mutations that alter the function of lysosome-related organelles. Pulmonary fibrosis is the major cause of morbidity and mortality in HPS-1 and HPS-4 patients. However, the mechanisms that underlie the exaggerated inj...

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Veröffentlicht in:	The Journal of immunology (1950) 2018-03, Vol.200 (6), p.2140-2153
Hauptverfasser:	Zhou, Yang, He, Chuan Hua, Yang, Daniel S, Nguyen, Tung, Cao, Yueming, Kamle, Suchitra, Lee, Chang-Min, Gochuico, Bernadette R, Gahl, William A, Shea, Barry S, Lee, Chun Geun, Elias, Jack A
Format:	Artikel
Sprache:	eng
Schlagworte:	Alveoli Animals Apoptosis Apoptosis - drug effects beta Catenin - metabolism Bleomycin Bleomycin - pharmacology Bronchoalveolar Lavage Fluid - chemistry Bronchus Cell Differentiation - drug effects Cell proliferation Cell Proliferation - drug effects Cell Proliferation - physiology Chitinase Chitinase-3-Like Protein 1 - metabolism Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Fibrosis Galectin 3 - metabolism Galectin-3 Hereditary diseases Hermanski-Pudlak Syndrome - metabolism Lung - drug effects Lung - metabolism Lung diseases Macrophages Macrophages - drug effects Macrophages - metabolism Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Morbidity Mutation Organelles Pulmonary Fibrosis - metabolism Rodents Wnt protein Wnt Signaling Pathway - drug effects β-Catenin
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