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ID 111456
著者
Song, Ying Jilin University|Nagoya University
Ishiguro, Hiroshi Nagoya University
Yamamoto, Akiko Nagoya University
Jin, Chun Xiang Jilin University
Kondo, Takaharu Nagoya University
キーワード
pancreatic duct cell
HCO3- transport
CFTR
slc26A6
資料タイプ
学術雑誌論文
抄録
Pancreatic duct epithelium secretes HCO3--rich fluid, which is dependent on cystic fibrosis transmembrane conductance regulator (CFTR). HCO3- transport across the apical membrane is thought to be mediated by both SLC26A6 Cl--HCO3- exchange and CFTR HCO3- conductance. In this study we examined the relative contribution and interaction of SLC26A6 and CFTR in apical HCO3- transport. Interlobular pancreatic ducts were isolated from slc26a6 null mice. Intracellular pH (pHi) was measured by BCECF microfluorometry. Duct cells were stimulated with forskolin and alkalinized by acetate pre-pulse in the presence ofHCO3--CO2. Apical HCO3- secretion was estimated from the recovery rate of pHi from alkaline load. When the lumen was perfused with high-Cl- solution, the rate of apical HCO3- secretion was increased by luminal application of CFTRinh-172 in ducts from wild-type mice but it was decreased in ducts from slc26a6 -/- mice. This suggests that slc26a6 and CFTR compensate/compete with each other for apical HCO3- secretion with high Cl- in the lumen. With high HCO3- in the lumen, luminal CFTRinh-172 reduced the rate of apical HCO3- secretion in both wild-type and slc26a6 -/- ducts. This suggests that HCO3- conductance of CFTR mediates a significant portion of apical HCO3- secretion with high HCO3- in the lumen.
掲載誌名
The Journal of Medical Investigation
ISSN
13496867
13431420
cat書誌ID
AA11166929
AA12022913
出版者
Faculty of Medicine Tokushima University
56
Supplement
開始ページ
332
終了ページ
335
並び順
332
発行日
2009-12
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版