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JCI online early table of contents: Jan. 10 2008
Date:1/10/2008

h and colleagues at Harvard Medical School, Boston, has revealed that these claudins interact synergistically, and that this interaction regulated the permeability of tight junctions to chloride molecules. FHHNC-causing mutant forms of either CLDN16 or CLDN19 disrupted this interaction and abolished the synergistic effect, providing important insights into the mechanisms underlying FHHNC.

TITLE: Claudin-16 and claudin-19 interact and form a cation-selective tight junction complex

AUTHOR CONTACT:
Daniel A Goodenough
Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 432-1652; Fax: (617) 432-2955; E-mail: daniel_goodenough@hms.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33970


HEPATOLOGY: Understanding how two drugs can be better than one for the treatment of a liver disease

Primary biliary cirrhosis (PBC) is a liver disease characterized by diminished expression of the liver protein AE2 and destruction of the bile ducts. The latter leads to a buildup of the waste product bile in the liver (a process known as cholestasis), which causes liver scarring and organ failure. The traditional treatment for PBC, administration of the bile acid ursodeoxycholic acid (UDCA), is ineffective for a subset of patients. However, these individuals often benefit from a combination treatment of glucocorticoid and UDCA, although the mechanisms underlying how either treatment alleviates PBC are poorly understood. In a new study, Juan Medina and his colleagues at the University of Navarra School of Medicine, Spain, have provided evidence for how UDCA and glucocorticoids work together to enhance AE2 activity in the liver.

Treatment of cultured human liver cells with a combination of UDCA and the glucocorticoid dexamethasone, but not with either trea
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Contact: Karen Honey
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Journal of Clinical Investigation
Source:Eurekalert

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