Angiotensin II participates in hepatic inflammation and fibrosis through MCP-1 expression
Digestive Diseases and Sciences, ISSN: 0163-2116, Vol: 50, Issue: 5, Page: 942-948
2005
- 47Citations
- 12Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations47
- Citation Indexes46
- 46
- CrossRef40
- Policy Citations1
- Policy Citation1
- Captures12
- Readers12
- 12
Article Description
In this study, we assessed the hypothesis that angiotensin (Ang) II could modulate inflammatory cell recruitment into the liver through hepatic expression of monocyte chemoattractant protein (MCP)-1 during liver injury. For in vivo study, Ang II type 1a knockout (AT1a KO) mice and wild-type (WT) mice were treated with CCl for 4 weeks. After CCl treatment, AT1a KO mice showed lower expression of MCP-1 and fewer CD68-positive cells in the liver compared with WT mice. For in vitro study, Ang II was added to LI90 cells. Ang II enhanced MCP-1 mRNA together with RhoA mRNA and also induced secretion of MCP-1 into the culture medium. This change was strongly blocked by Y-27632, a specific Rho-kinase inhibitor. These results suggest that Ang II modulates hepatic inflammation via production of MCP-1 by hepatic stellate cells, and the effect of Ang II on MCP-1 production is, at least partly, mediated by the Rho/Rho-kinase pathway. © 2005 Springer Science+Business Media, Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=18844457924&origin=inward; http://dx.doi.org/10.1007/s10620-005-2669-7; http://www.ncbi.nlm.nih.gov/pubmed/15906773; http://link.springer.com/10.1007/s10620-005-2669-7; https://dx.doi.org/10.1007/s10620-005-2669-7; https://link.springer.com/article/10.1007/s10620-005-2669-7; http://www.springerlink.com/index/10.1007/s10620-005-2669-7; http://www.springerlink.com/index/pdf/10.1007/s10620-005-2669-7
Springer Science and Business Media LLC
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