title: Cystic fibrosis transmembrane conductance regulator and Na+ channel subunits mRNA transcripts, and Cl- efflux, show a different distribution in rat duodenum and colon.
abstract: OBJECTIVE
  We compared the distribution and putative association of Cl- channel transport, CFTR mRNA transcripts, and Na+ channel (ENaC) alpha- and beta-subunit mRNA transcripts in villus and crypt epithelial cells of duodenum, with corresponding surface and crypt cells of colon from sodium-depleted rats.
  
  
  METHODS
  Cells were loaded with 36Cl- and forskolin-stimulated efflux was determined. RT-PCR was performed for CFTR mRNA transcripts and ENaC alpha- and beta-subunit mRNA. Duodenal epithelial cell response to VIP was assessed by measuring intracellular cAMP.
  
  
  RESULTS
  Forskolin-stimulated Cl- efflux occurred with decreasing magnitude in duodenal crypt, duodenal villus, colonic crypt and colonic surface cells in Na(+)-depleted animals. CFTR expression was correlated directly with Cl- efflux (r=0.91, P<0.01). Na+ channel alpha-subunit was expressed in colon and duodenum in animals fed diets with a high or low sodium content. While the beta-subunit mRNA was detected in the colon of sodium-restricted rats, it was absent in the duodenum under control conditions and after Na+ restriction. There was an inverse correlation between mRNA transcripts for CFTR and the ENaC alpha-subunit (r=-0.93, P<0.003) and beta-subunit (r=-0.91, P<0.004) in colon. VIP-stimulated cAMP in duodenal epithelial cells was greater in crypt than villus (P<0.05).
  
  
  CONCLUSIONS
  Cl- efflux, CFTR transcription and forskolin-stimulated cAMP activity occur in both crypt and villus epithelial cells in duodenum. Possible interaction between CFTR and Na+ channels is apparently limited to parts of the colonic crypt. Lack of duodenal beta-subunit expression makes ENaC activity unlikely.
authors.affiliation: Department of Gastroenterology, Soroka Medical Center and Ben Gurion University of the Negev, Beer Sheva, Israel.
authors.forename: H S
authors.initials: HS
authors.lastname: Odes
authors.forename: P
authors.initials: P
authors.lastname: Smirnoff
authors.forename: R
authors.initials: R
authors.lastname: Guberman
authors.forename: S
authors.initials: S
authors.lastname: Pollak-Charcon
authors.forename: A D
authors.initials: AD
authors.lastname: Sperber
authors.forename: A
authors.initials: A
authors.lastname: Fich
authors.forename: G M
authors.initials: GM
authors.lastname: Fraser
authors.forename: B
authors.initials: B
authors.lastname: Schwartz
mesh_terms: D000818:Animals; D001692:Biological Transport / Q000502:physiology; D018118:Chloride Channels / Q000032:analysis*; D005576:Colforsin / Q000494:pharmacology; D003106:Colon / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000242:Cyclic AMP / Q000096:biosynthesis; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000032:analysis*; D004386:Duodenum / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D015222:Sodium Channels / Q000032:analysis*
chemical_list: D018118:Chloride Channels; D012333:RNA, Messenger; D015222:Sodium Channels; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D005576:Colforsin; D000242:Cyclic AMP