An essential role for CCAAT/enhancer binding protein Β in bleomycin-induced pulmonary fibrosis No conflicts of interest were declared.

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dc.contributor.author Hu, B. en_US
dc.contributor.author Ullenbruch, M. R. en_US
dc.contributor.author Jin, H. en_US
dc.contributor.author Gharaee-Kermani, M. en_US
dc.contributor.author Phan, S. H. en_US
dc.date.accessioned 2007-09-20T18:09:20Z
dc.date.available 2008-04-03T18:48:55Z en_US
dc.date.issued 2007-03 en_US
dc.identifier.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> en_US
dc.identifier.issn 0022-3417 en_US
dc.identifier.issn 1096-9896 en_US
dc.identifier.uri http://hdl.handle.net/2027.42/55933
dc.identifier.uri http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17177178&dopt=citation en_US
dc.description.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. en_US
dc.format.extent 766960 bytes
dc.format.extent 3118 bytes
dc.format.mimetype application/pdf
dc.format.mimetype text/plain
dc.publisher John Wiley & Sons, Ltd. en_US
dc.subject.other Life and Medical Sciences en_US
dc.subject.other Cancer Research, Oncology and Pathology en_US
dc.title An essential role for CCAAT/enhancer binding protein Β in bleomycin-induced pulmonary fibrosis No conflicts of interest were declared. en_US
dc.type Article en_US
dc.rights.robots IndexNoFollow en_US
dc.subject.hlbsecondlevel Pathology en_US
dc.subject.hlbtoplevel Health Sciences en_US
dc.description.peerreviewed Peer Reviewed en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA en_US
dc.contributor.affiliationum Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA en_US
dc.contributor.affiliationum Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA ; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA. en_US
dc.identifier.pmid 17177178 en_US
dc.description.bitstreamurl http://deepblue.lib.umich.edu/bitstream/2027.42/55933/1/2119_ftp.pdf en_US
dc.identifier.doi http://dx.doi.org/10.1002/path.2119 en_US
dc.identifier.source The Journal of Pathology en_US
dc.owningcollname Interdisciplinary and Peer-Reviewed
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