Chloride-bicarbonate exchangers in the human fetal pancreas

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

doi:10.1006/bbrc.1999.1367

Chloride-bicarbonate exchangers in the human fetal pancreas

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

^*Corresponding author for this work

Pediatrics

Research output: Contribution to journal › Article › peer-review

11 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 language	English (US)
Pages (from-to)	315-321
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	263
Issue number	2
DOIs	https://doi.org/10.1006/bbrc.1999.1367
State	Published - Sep 24 1999

Funding

Grant support: DK46589 from the National Institutes of Health, U.S.A., and the Cystic Fibrosis Trust, UK. 1Current address: Nuffield Department of Surgery, Oxford University. 2To whom correspondence should be addressed. Fax: 44-1865-222626. E-mail: [email protected].

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1006/bbrc.1999.1367

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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.",

author = "Karen Hyde and Deborah Harrison and Hollingsworth, {Michael A.} and Ann Harris",

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N2 - 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.

AB - 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.

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Chloride-bicarbonate exchangers in the human fetal pancreas

Abstract

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