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secretion
Department of Integrative Biology, Pharmacology and Physiology, and Department of Internal Medicine, Division of Gastroenterology, Hepatology and Nutrition, The University of Texas Health Science Center at Houston, Medical School, Houston, Texas 77030
Fluid transport in the large intestine is mediated by the
cystic fibrosis gene product and cAMP-dependent anion channel cystic fibrosis transmembrane conductance regulator (CFTR). cAMP-mediated Cl
secretion by gastrointestinal cell lines
in vitro has been positively correlated with the insertion of CFTR
into the apical membrane of differentiated senescent colonocytes and
negatively correlated with the failure of CFTR to insert into the
plasma membrane of their undifferentiated proliferating counterparts.
In native tissues, this relationship remains unresolved. We
demonstrate, in a transmissible murine colonic hyperplasia (TMCH)
model, that (8-fold) colonocyte proliferation was accompanied by
increased cellular CFTR mRNA and protein expression (8.3- and 2.4-fold,
respectively) and enhanced mucosal cAMP-dependent Cl
secretion (2.3-fold). By immunofluorescence microscopy, cellular CFTR
expression was restricted to the apical pole of cells at the base of
the epithelial crypt. In contrast, increased cellular proliferation in
vivo led to increases in both the cellular level and the total number
of cells expressing this anion channel, with cellular CFTR staining
extending into the crypt neck region. Hyperproliferating colonocytes
accumulated large amounts of CFTR in apically oriented subcellular
perinuclear compartments. This novel mode of CFTR regulation may
explain why high endogenous levels of cellular CFTR mRNA and protein
within the TMCH epithelium were not matched with larger increases in
transmucosal CFTR Cl current.
cystic fibrosis transmembrane conductance regulator; regulation; location; mRNA; protein
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