Chloride-bicarbonate exchangers in the human fetal pancreas

Karen Hyde, Deborah Harrison, Michael A. Hollingsworth, Ann Harris

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene that encodes a small conductance cAMP-activated chloride ion channel. In the CF pancreatic duct, mutations in CFTR cause a reduction in bicarbonate secretion. This is thought to result from CFTR operating in parallel with a chloride-bicarbonate (Cl-/HCO3-) exchanger, located in the apical membrane of pancreatic duct cells. The molecular basis of this Cl-/HCO3- exchanger has not been identified. A combination of screening cDNA libraries, RNase protection, and 5' RACE analysis was used to identify Cl-/HCO3- exchangers in human fetal pancreas. An AE2 Cl-/HCO3- exchanger was shown to be expressed in human fetal pancreas from the midtrimester of gestation, at a time when CF-associated pathology commences. In addition, an AE1 Cl-/HCO3- was identified in fetal pancreas but was absent from the adult pancreas and cultured ductal epithelial cells from fetal and adult pancreas.

Original languageEnglish (US)
Pages (from-to)315-321
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume263
Issue number2
DOIs
StatePublished - Sep 24 1999

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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