CX3CL1-CX3CR1 interaction prevents carbon tetrachloride-induced liver inflammation and fibrosis in mice†
Version of Record online: 11 JUN 2010
Copyright © 2010 American Association for the Study of Liver Diseases
Volume 52, Issue 4, pages 1390–1400, October 2010
How to Cite
Aoyama, T., Inokuchi, S., Brenner, D. A. and Seki, E. (2010), CX3CL1-CX3CR1 interaction prevents carbon tetrachloride-induced liver inflammation and fibrosis in mice. Hepatology, 52: 1390–1400. doi: 10.1002/hep.23795
Potential conflict of interest: Nothing to report.
- Issue online: 11 JUN 2010
- Version of Record online: 11 JUN 2010
- Manuscript Accepted: 1 JUN 2010
- Manuscript Received: 22 JAN 2010
- Liver Scholar Award from the American Association for the Study of Liver Diseases and the American Liver Foundation
- Alcoholic Beverage Medical Research Foundation
- pilot project of the Southern California Research Center for Alcoholic Liver and Pancreatic Diseases and Cirrhosis. Grant Number: P50 AA11999
- National Institute on Alcohol Abuse and Alcoholism
- National Institutes of Health. Grant Number: 5R01GM041804
Additional Supporting Information may be found in the online version of this article.
|HEP_23795_sm_SuppFig1.tif||4681K||Supporting Information Figure 1. No alterations of oxidant stress and CYP2E1 expression between WT and CX3CR1-deficient mice after CCl4 treatment. (A) Immunofluorescence for 4-hydroxy-nonenal (4-HNE)(original magnification: x200) and (B) Western blot for CYP2E1 in the livers from WT and CX3CR1-deficient mice after 12 injections of vehicle or CCl4 are shown.|
|HEP_23795_sm_SuppFig2.tif||3224K||Supporting Information Figure 2. AKT and ERK are required for CX3CL1-induced anti-inflammatory properties. WT Kupffer cells were pretreated with LY294002 (AKT inhibitor, 2 μM) or U0125 (ERK inhibitor, 20 μM) for 30 min, followed by treating with CX3CL1 (100 ng/ml) for additional 6 h. mRNA expression of IL-10 and arginase-1 was measured by qPCR. *p<;0.05, N.S. not significant.|
|HEP_23795_sm_SuppFig3.tif||3299K||Supporting Information Figure 3. CX3CL1 treatment inhibits LPS-induced cytokine production in Kupffer cells. WT Kupffer cells were treated with LPS (10 ng/ml) for 6 h, in the presence or absence of CX3CL1 (100 ng/ml). mRNA expression of TNF-α and TGF-β was measured by qPCR. *p<0.05,|
|HEP_23795_sm_SuppFig4.tif||4885K||Supporting Information Figure 4. CX3CR1 expression in hepatic NK cells and T cells. Liver mononuclear cells isolated from vehicle or CCl4-treated CX3CR1+/GFP mice, were stained with anti-NK1.1 and CD3 antibody followed by FACS analysis for detecting the expression of NK1.1, CD3 and GFP as endogenous CX3CR1 expression. Representative FACS analysis is shown (n=3).|
|HEP_23795_sm_SuppTable1.doc||21K||Supporting Information Table 1.|
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