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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Duitman, JanWillem Borensztajn, Keren S. Pulskens, Willem P. C. Leemans, Jaklien C. Florquin, Sandrine Spek, C. Arnold |
| Description | Country affiliation: Netherlands Author Affiliation: Duitman J ( Center for Experimental and Molecular Medicine (CEMM), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.); Borensztajn KS ( Unité INSERM 700, Physiopathologie et Epidémiologie de l'Insuffisance Respiratoire, Faculté de Médecine Xavier Bichat, Paris, France.); Pulskens WP ( Department of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.); Leemans JC ( Department of Pathology); Florquin S ( 1] Department of Pathology); Spek CA ( Center for Experimental and Molecular Medicine (CEMM), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.) |
| Abstract | CCAAT-enhancer-binding protein delta (C/EBPδ) is a transcription factor mainly known for its role in inflammation and apoptosis/proliferation. Considering that these are key processes in renal fibrosis, we hypothesized that C/EBPδ would potentiate renal fibrosis. In line with this hypothesis, C/EBPδ has recently been suggested to regulate the fibrotic response during glomerulonephritis. Here we determined the importance of C/EBPδ in the development of renal tubulointerstitial fibrosis by subjecting 8- to 12-week-old C/EBPδ-deficient mice and age- and sex-matched wild-type controls to the unilateral ureteral obstruction model. Mice were killed at 1, 3, or 7 days post surgery, and renal tissues were obtained for RNA, protein, and immunohistochemical analysis. We show that C/EBPδ deficiency resulted in a more profound fibrotic response as evident from enhanced tubular injury, collagen deposition in the interstitial area, and higher expression of transforming growth factor-ß. Moreover, we show that the increase in renal fibrosis in C/EBPδ-deficient mice does not depend on an altered proliferation/apoptosis balance or on a differential inflammatory response in the obstructed kidney. In conclusion, our study provides direct evidence that C/EBPδ is a novel mediator of renal fibrosis. Modulating C/EBPδ expression could consequently be a potential antifibrotic strategy in patients with chronic kidney disease. |
| File Format | HTM / HTML |
| ISSN | 00236837 |
| Issue Number | 1 |
| Volume Number | 94 |
| e-ISSN | 15300307 |
| Journal | Laboratory Investigation |
| Language | English |
| Publisher | Nature Publishing Group |
| Publisher Date | 2014-01-01 |
| Publisher Place | United States |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Pathology Ccaat-enhancer-binding Protein-delta Metabolism Kidney Tubules Pathology Renal Insufficiency, Chronic Animals Apoptosis Genetics Cell Growth Processes Physiology Female Fibrosis Immunohistochemistry Mice Mice, Inbred C57bl Mice, Transgenic Statistics, Nonparametric Ureteral Obstruction Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Molecular Biology Pathology and Forensic Medicine |
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