Show simple item record

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

dc.contributor.authorHu, Bernadineen_US
dc.contributor.authorUllenbruch, M. R.en_US
dc.contributor.authorJin, H.en_US
dc.contributor.authorGharaee-Kermani, M.en_US
dc.contributor.authorPhan, Sem H.en_US
dc.date.accessioned2007-09-20T18:09:20Z
dc.date.available2008-04-03T18:48:55Zen_US
dc.date.issued2007-03en_US
dc.identifier.citationHu, 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.issn0022-3417en_US
dc.identifier.issn1096-9896en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/55933
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17177178&dopt=citationen_US
dc.description.abstractPulmonary 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.extent766960 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherJohn Wiley & Sons, Ltd.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherCancer Research, Oncology and Pathologyen_US
dc.titleAn essential role for CCAAT/enhancer binding protein Β in bleomycin-induced pulmonary fibrosis No conflicts of interest were declared.en_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPathologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment 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.pmid17177178en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/55933/1/2119_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/path.2119en_US
dc.identifier.sourceThe Journal of Pathologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Show simple item record

Accessibility: If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.