XXXX shuts down calcium signaling in cholangiocytes.

@entity1 @entity671 @entity268 @entity35 @entity409 @entity3157 @entity1448 @entity74 @entity141 @entity253 @entity15304
BACKGROUND _ AIMS: @entity1448 is one of the principal manifestations of @entity409 and often results from disorders involving bile duct epithelia rather than hepatocytes. @entity74 affects @entity253 , and no unifying pathophysiologic event in these cells has been identified as the cause of @entity1448 . Here we examined the role of the @entity671 receptor ( @entity15304 )/ @entity141 release channel in @entity141 signaling and ductular secretion in animal models of @entity1448 and in @entity1 with @entity1448 . METHODS: The expression and distribution of the @entity15304 and related proteins were examined in @entity35 cholangiocytes before and after bile duct ligation or treatment with endotoxin. @entity141 signaling was examined in isolated bile ducts from these animals, whereas ductular @entity3157 secretion was examined in isolated perfused livers. Confocal immunofluorescence was used to examine cholangiocyte @entity15304 expression in @entity1 liver biopsy specimens. RESULTS: Expression of the @entity15304 was selectively lost from @entity253 after bile duct ligation or endotoxin treatment. As a result, @entity141 signaling and @entity141 -mediated @entity3157 secretion were lost as well, although other components of the @entity141 signaling pathway and @entity268 ( @entity268 )-mediated @entity3157 secretion both were preserved. Examination of @entity1 liver biopsy specimens showed that InsP3Rs also were lost from bile duct epithelia in a range of @entity1 @entity1448 , although @entity15304 expression was intact in noncholestatic @entity409 . CONCLUSIONS: @entity15304 -mediated @entity141 signaling in bile duct epithelia appears to be important for normal bile secretion in the liver, and loss of InsP3Rs may be a final common pathway for @entity1448 .
