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Am J Physiol Gastrointest Liver Physiol (November 10, 2005). doi:10.1152/ajpgi.00308.2005
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Submitted on July 6, 2005
Accepted on November 6, 2005

Secretion of MCP-1/CCL2 by Bile Duct Epithelia Induces Myofibroblastic Transdifferentiation of Portal Fibroblasts

Emma A. Kruglov1, Rebecca A. Nathanson1, Trong Nguyen1, and Jonathan A. Dranoff1*

1 Section of Digestive Diseases and Yale Liver Center, Yale University School of Medicine, New Haven, CT, USA

* To whom correspondence should be addressed. E-mail: jonathan.dranoff{at}yale.edu.

Portal fibroblasts (PF) are fibrogenic liver cells distinct from hepatic stellate cells (HSC). Recent evidence suggests that PF may be important mediators of biliary fibrosis and cirrhosis. The cytokine MCP-1/CCL2 is upregulated in biliary fibrosis by bile duct epithelia (BDE) and induces functional responses in HSC. Thus, we hypothesized that release of MCP-1 may mediate biliary fibrosis. Here we report that PF express functional receptors for MCP-1 that are distinct from CCR2. MCP-1 induces proliferation, increase and redistribution of {alpha}-smooth muscle ({alpha}-SMA) expression, loss of NTPDase2, and upregulation of {alpha}(1)-procollagen production in PF. BDE secretions induce {alpha}-SMA levels in PF, and this is inhibited by MCP-1 blocking antibody. Taken together, these data suggest that BDE regulate PF proliferation and myofibroblastic transdifferentiation in a paracrine fashion via release of MCP-1.




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