Phillip C. Bost

Works (1)

Updated: July 5th, 2023 15:53

2008 journal article

STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loop

JOURNAL OF IMMUNOLOGY, 180(6), 4200–4207.

By: A. Antao-Menezes*, E. Turpin*, P. Bost n, J. Ryman-Rasmussen n & J. Bonner n 

MeSH headings : Autocrine Communication / drug effects; Autocrine Communication / immunology; Cell Line; Culture Media, Conditioned; Enzyme Inhibitors / pharmacology; Fibroblasts / drug effects; Fibroblasts / enzymology; Fibroblasts / immunology; Fibroblasts / metabolism; Humans; Hydrogen Peroxide / metabolism; Interferon-beta / physiology; Intracellular Fluid / drug effects; Intracellular Fluid / immunology; Intracellular Fluid / metabolism; Lung / drug effects; Lung / enzymology; Lung / immunology; Lung / metabolism; NADPH Oxidases / antagonists & inhibitors; NADPH Oxidases / physiology; Phosphorylation; Reactive Oxygen Species / metabolism; STAT1 Transcription Factor / metabolism; STAT1 Transcription Factor / physiology; Signal Transduction / drug effects; Signal Transduction / immunology; Vanadium Compounds / pharmacology; Xanthine Oxidase / physiology
TL;DR: Fibroblasts play a role in the innate immune response to vanadium-induced oxidative stress by synthesizing IFN-β and activating STAT-1 to cause growth arrest and increase levels of CXCL10, a potent antifibrotic factor. (via Semantic Scholar)
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Added: August 6, 2018

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