An essential role for CCAAT/enhancer binding protein Β in bleomycin-induced pulmonary fibrosis No conflicts of interest were declared.
dc.contributor.author | Hu, Bernadine | 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, Sem 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 | https://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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