BAX inhibitor-1-associated V-ATPase glycosylation enhances collagen degradation in pulmonary fibrosis.
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ABSTRACT:
SUBMITTER: Lee MR
PROVIDER: S-EPMC3973240 | biostudies-literature | 2014 Mar
REPOSITORIES: biostudies-literature
Publications
BAX inhibitor-1-associated V-ATPase glycosylation enhances collagen degradation in pulmonary fibrosis.
Lee M-R MR Lee G-H GH Lee H-Y HY Kim D-S DS Chung M J MJ Lee Y C YC Kim H-R HR Chae H-J HJ
Cell death & disease 20140313
Endoplasmic reticulum (ER) stress is considered one of the pathological mechanisms of idiopathic pulmonary fibrosis (IPF). Therefore, we examined whether an ER stress regulator, Bax inhibitor-1 (BI-1), regulates collagen accumulation, which is both a marker of fibrosis and a pathological mechanism of fibrosis. The presence of BI-1 inhibited the transforming growth factor-β1-induced epithelial-mesenchymal transition of epithelial pulmonary cells and bleomycin-induced pulmonary fibrosis in a mouse ...[more]
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