دورية أكاديمية
An essential role for CCAAT/enhancer binding protein beta in bleomycin-induced pulmonary fibrosis.
| العنوان: | An essential role for CCAAT/enhancer binding protein beta in bleomycin-induced pulmonary fibrosis. |
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| المؤلفون: | Hu B; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109-2200, USA., Ullenbruch MR, Jin H, Gharaee-Kermani M, Phan SH |
| المصدر: | The Journal of pathology [J Pathol] 2007 Mar; Vol. 211 (4), pp. 455-62. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: John Wiley And Sons Country of Publication: England NLM ID: 0204634 Publication Model: Print Cited Medium: Print ISSN: 0022-3417 (Print) Linking ISSN: 00223417 NLM ISO Abbreviation: J Pathol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Chichester : John Wiley And Sons Original Publication: London, Oliver & Boyd. |
| مواضيع طبية MeSH: | CCAAT-Enhancer-Binding Protein-beta/*analysis , Pulmonary Fibrosis/*metabolism, Actins ; Animals ; Antibiotics, Antineoplastic ; Bleomycin ; CCAAT-Enhancer-Binding Protein-beta/deficiency ; Cell Differentiation/physiology ; Cell Division/physiology ; Cells, Cultured ; Collagen/analysis ; Cytokines/analysis ; Fibroblasts/physiology ; Gene Expression ; Genotype ; Lung/pathology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth/metabolism ; Pulmonary Fibrosis/pathology ; Pulmonary Fibrosis/physiopathology ; RNA, Messenger/analysis |
| مستخلص: | 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 beta (C/EBPbeta) 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/EBPbeta in the development of pulmonary fibrosis, experiments using C/EBPbeta null mice and their wild-type littermates were conducted. Our findings indicated that, compared to wild-type mice, animals deficient in C/EBPbeta showed significantly reduced fibrotic lesions and collagen deposition in the lung upon endotracheal injection of bleomycin. Further studies on the mechanisms by which C/EBPbeta regulates fibrosis indicated that knockout of C/EBPbeta attenuates inflammatory cytokine expression in bleomycin-treated mice. The reduced alpha-smooth muscle actin gene expression in either isolated lung fibroblasts or lung tissue from bleomycin or saline-treated C/EBPbeta deficient mice suggests that C/EBPbeta regulates myofibroblast differentiation during fibrosis. Consistent with this finding, cells from C/EBPbeta deficient mice exhibited higher proliferative rates than those from wild-type mice. These data suggest that C/EBPbeta 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 (c) 2006 Pathological Society of Great Britain and Ireland.) |
| معلومات مُعتمدة: | HL28737 United States HL NHLBI NIH HHS; HL31963 United States HL NHLBI NIH HHS; HL52285 United States HL NHLBI NIH HHS; HL77297 United States HL NHLBI NIH HHS |
| المشرفين على المادة: | 0 (Actins) 0 (Antibiotics, Antineoplastic) 0 (CCAAT-Enhancer-Binding Protein-beta) 0 (Cytokines) 0 (RNA, Messenger) 11056-06-7 (Bleomycin) 9007-34-5 (Collagen) |
| تواريخ الأحداث: | Date Created: 20061221 Date Completed: 20070424 Latest Revision: 20071203 |
| رمز التحديث: | 20221213 |
| DOI: | 10.1002/path.2119 |
| PMID: | 17177178 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 0022-3417 |
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| DOI: | 10.1002/path.2119 |