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Articles in PresS, published online ahead of print January 16, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00298.2001
Submitted on July 11, 2001
Accepted on January 8, 2002
1 Department fo Physiological Sciences, Pontificia Universidad Catolica de Chile, Santiago, Chile
2 Department of Gastroenterology, Pontificia Universidad Catolica de Chile, Santiago, Chile
* To whom correspondence should be addressed. E-mail: hegonzal{at}mdanderson.org.
Hepatocyte gap junctional proteins, connexins (Cxs) 26 and 32, are down regulated during obstructive cholestasis (OC) and lipopolysaccharide hepatocellular cholestasis (LPS-HC). We investigated rat hepatic Cxs during ethynylestradiol hepatocellular cholestasis (EE-HC) and choledochocaval fistula (CCF) and compared them with OC and LPS-HC. Levels (immunoblotting) and cellular distribution (immunofluorescence) of Cxs 26, 32 and 43, as well as macrophage infiltration, were studied in livers of rats under each condition. Connexins 26 and 32 were reduced in LPS-HC, OC and CCF. However, in EE-HC Cx26 did not change and Cx32 was increased. Prominent inflammation occurred in LPS-HC, OC and CCF, which was associated with increased levels of Cx43 in LPS-HC and OC, but not CCF. No inflammation nor changes in Cx43 levels occurred during EE-HC. In cultured hepatocytes, dye coupling was reduced by TNF-
, IL-1ß, IL-6, while reduction induced by LPS required co-culture with Kupffer cells. Thus, hepatocyte gap junctions are down regulated in forms of cholestasis associated with inflammation, and reduced intercellular communication might be induced in part by proinflammatory mediators.
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