An essential role for CCAAT/enhancer binding protein Β in bleomycin-induced pulmonary fibrosis No conflicts of interest were declared.
Hu, Bernadine; Ullenbruch, M. R.; Jin, H.; Gharaee-Kermani, M.; Phan, Sem H.
2007-03
Citation
Hu, B; Ullenbruch, MR; Jin, H; Gharaee-Kermani, M; Phan, SH (2007). "An essential role for CCAAT/enhancer binding protein Β in bleomycin-induced pulmonary fibrosis No conflicts of interest were declared. ." The Journal of Pathology 211(4): 455-462. <http://hdl.handle.net/2027.42/55933>
Abstract
Pulmonary fibrosis is characterized by inflammation, genesis of myofibroblasts, and abnormal tissue repair. Despite extensive research, its pathogenesis remains incompletely understood. Previously, the transcription factor CCAAT/enhancer binding protein Β (C/EBPΒ) was found to be a key regulator of myofibroblast differentiation in vitro , and to be involved in the acute phase and inflammatory responses. In an attempt to test the role of C/EBPΒ in the development of pulmonary fibrosis, experiments using C/EBP Β null mice and their wild-type littermates were conducted. Our findings indicated that, compared to wild-type mice, animals deficient in C/EBPΒ showed significantly reduced fibrotic lesions and collagen deposition in the lung upon endotracheal injection of bleomycin. Further studies on the mechanisms by which C/EBPΒ regulates fibrosis indicated that knockout of C/EBP Β attenuates inflammatory cytokine expression in bleomycin-treated mice. The reduced Α-smooth muscle actin gene expression in either isolated lung fibroblasts or lung tissue from bleomycin or saline-treated C/EBPΒ deficient mice suggests that C/EBPΒ regulates myofibroblast differentiation during fibrosis. Consistent with this finding, cells from C/EBPΒ deficient mice exhibited higher proliferative rates than those from wild-type mice. These data suggest that C/EBPΒ plays an essential role in pulmonary fibrosis and that this role appears to be multifactorial with respect to cytokine expression, cell differentiation, and proliferation. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.Publisher
John Wiley & Sons, Ltd.
ISSN
0022-3417 1096-9896
Other DOIs
PMID
17177178
Types
Article
URI
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17177178&dopt=citationMetadata
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