These authors contributed equally to this article.
Osteopontin is a novel downstream target of SOX9 with diagnostic implications for progression of liver fibrosis in humans†
Version of Record online: 28 AUG 2012
Copyright © 2012 American Association for the Study of Liver Diseases
Volume 56, Issue 3, pages 1108–1116, September 2012
How to Cite
Pritchett, J., Harvey, E., Athwal, V., Berry, A., Rowe, C., Oakley, F., Moles, A., Mann, D. A., Bobola, N., Sharrocks, A. D., Thomson, B. J., Zaitoun, A. M., Irving, W. L., Guha, I. N., Hanley, N. A. and Hanley, K. P. (2012), Osteopontin is a novel downstream target of SOX9 with diagnostic implications for progression of liver fibrosis in humans. Hepatology, 56: 1108–1116. doi: 10.1002/hep.25758
Potential conflict of interest: Nothing to report.
- Issue online: 28 AUG 2012
- Version of Record online: 28 AUG 2012
- Accepted manuscript online: 5 APR 2012 12:00AM EST
- Manuscript Accepted: 26 MAR 2012
- Manuscript Received: 7 SEP 2011
- Medical Research Council (MRC)
- Manchester National Institutes of Health Research Biomedical Research Center and Stem Cells for Safer Medicine
- Wellcome Trust Senior Fellow in Clinical Science
- Royal Society-Wolfson research merit award
- MRC Clinical Training Fellow
- Biotechnology and Biological Sciences Research Council doctoral account Ph.D. studentship
Additional Supporting Information may be found in the online version of this article.
|HEP_25758_sm_SuppFig1.tif||6392K||Supporting Information Figure 1. Immunohistochemistry of SOX9 and OPN in normal mouse liver. Consecutive 5 μm sections of normal liver in mouse stained for SOX9 and OPN (brown), counterstained with toludine blue. Detection only in the round nuclei (SOX9) and cytoplasm (OPN) of biliary epithelial cells. Size bar represents 50 μm|
|HEP_25758_sm_SuppFig2.tif||685K||Supporting Information Figure 2. Sox9 and Opn detection in activated HSCs. A, Example immunoblot showing increased Sox9 and Opn in activated (A) compared to quiescent (Q) rat HSCs (rHSCs). B, Quantification of Sox9 and Opn in quiescent and activated rHSCs detected by immunoblotting. Immunoblotting quantification was normalized to β-actin. **, p<0.01, †, p<0.005.|
|HEP_25758_sm_SuppFig3.tif||159K||Supporting Information Figure 3. PCR for an intergenic region of GAPDH (i.e. no Sox9 binding motif) as a negative control for the ChIP assay shown in Figure 4. Positive control is input (diluted 10-fold). No PCR product is seen following immunoprecipitation using anti-Sox9 (or negative control IgG) antibodies.|
|HEP_25758_sm_SuppFig4.tif||2893K||Supporting Information Figure 4. A and B, Example immunoblots showing decrease and increase in OPN and SOX9 following cyclopamine or SAG treatment respectively (relating to experiments in Fig. 6B and D). C, Example immunoblot for Fig. 6E). D, Control data for Fig. 6F to demonstrate that transient transfection of the SOX9 cDNA expression vector produces increased levels of SOX9 in the presence of cyclopamine (CYC) in LX2 cells. Quantification of SOX9 protein was normalized to β-actin. †, p<0.005 compared to empty vector (EV) / DMSO treated control.|
|HEP_25758_sm_SuppFig5.tif||475K||Supporting Information Figure 5. A and B, example immunoblots and verification of myc-tagged GLI2?N and GLI3A expression in cells following transfection. EV, empty vector control.|
|HEP_25758_sm_SuppTabs.doc||67K||Supporting Information Tables.|
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