PMID: 8944687Nov 1, 1996Paper

Progesterone and estradiol inhibit CFTR-mediated ion transport by pancreatic epithelial cells

The American Journal of Physiology
N B SweezeyH Kopelman

Abstract

The cystic fibrosis (CF), gene product, CF transmembrane conductance regulator (CFTR), is responsible for adenosine 3',5'-cyclic monophosphate (cAMP)-activated Cl- transport in epithelial cells, and mutant CFTR accounts for the pathology in the CF pancreas. We have previously shown that both isolated rabbit pancreatic acini and the human pancreatic duct cell line PANC-1 possess a cAMP-activated Cl- conductance identified as CFTR. We report here that preincubation in either of the female hormones progesterone or beta-estradiol inhibits activation by cAMP, but not by Ca2+ ionophore, of PANC-1 cell volume reduction under isotonic conditions. cAMP-activated cell volume reduction is sensitive to antisense, but not sense, CFTR oligodeoxynucleotide. Furthermore, progesterone inhibits cAMP-activated Cl- efflux from rabbit acinar cells. Moreover preincubation with progesterone, but not beta-estradiol, reduces CFTR mRNA and protein levels as measured using polymerase chain reaction amplification of reverse-transcribed acinar RNA and Western blots of protein from acinar membranes. We conclude that female hormones inhibit CFTR functional activity in pancreatic epithelial cells by different mechanisms.

Citations

Apr 10, 2010·American Journal of Respiratory and Critical Care Medicine·Sanjay H ChotirmallNoel G McElvaney
Oct 29, 2000·American Journal of Physiology. Gastrointestinal and Liver Physiology·K KlingelF Lang
Oct 14, 2006·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Joseph R ShawBruce A Stanton
Feb 13, 2020·International Journal of Molecular Sciences·Gaetano RiemmaPasquale De Franciscis
Oct 9, 2004·Human Reproduction·Xiao-Ying ZhengHai-Yan Wang

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