BBC3 in macrophages promoted pulmonary fibrosis development through inducing autophagy during silicosis.

ABSTRACT: Following inhalation into the lungs, silica particles are engulfed by alveolar macrophages, which triggers endogenous or exogenous apoptosis signaling pathways. As an inducer of apoptosis, the role of BBC3/PUMA (BCL2-binding component 3) in macrophages during silicosis remains unknown. Here, we exposed U937 cell-derived macrophages (UDMs) to SiO₂ in vitro to explore the function of BBC3 in SiO₂-induced disease. We found that SiO₂ induced increased BBC3 expression, as well as macrophage activation and apoptosis. Knockdown of Bbc3 with specific siRNA significantly mitigated the SiO₂-induced effects. In addition, our results clearly showed increased levels of autophagy in macrophages exposed to SiO₂. However, inhibition of BBC3 decreased

SUBMITTER: Liu H 

PROVIDER: S-EPMC5386570 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature