Does ursodeoxycholic acid stimulate cholangiocyte fluid secretion in mice via CFTR-dependent ATP secretion?
Our data indicate that UDCA stimulates a CFTR-dependent apical ATP release in cholangiocytes. Secreted ATP activates purinergic 2Y receptors, and, through [Ca(2+)]i increase and PKC activation stimulates Cl(-) efflux and fluid secretion. These data support the concept that CFTR plays a role in modulating purinergic signaling in secretory epithelia and suggest a novel mechanism explaining the choleretic effect of UDCA.
Both clinical and socioeconomic risk factors should be used to target women at risk. In terms of the quality of care, this study links clinical and socioeconomic risk factors to poor outcomes. Further studies are needed, however, to link the quality of care at various locations to these outcomes.