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Am J Physiol Cell Physiol 284: C729-C737, 2003. First published November 20, 2002; doi:10.1152/ajpcell.00166.2002
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Vol. 284, Issue 3, C729-C737, March 2003

Localization of Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> cotransporter (NBC-1) variants in rat and human pancreas

Hiroaki Satoh1, Nobuo Moriyama2, Chiaki Hara1, Hideomi Yamada1, Shoko Horita1, Motoei Kunimi1, Kazuhisa Tsukamoto1, Naoyuki Iso-o1, Jun Inatomi3, Hayato Kawakami4, Akihiko Kudo4, Hitoshi Endou3, Takashi Igarashi5, Atsuo Goto1, Toshiro Fujita1, and George Seki1

Departments of 1 Internal Medicine, 2 Hemodialysis and Apheresis, and 5 Pediatrics, Faculty of Medicine, Tokyo University Tokyo 113-0033; and Departments of 3 Pharmacology and Toxicology, and 4 Anatomy, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan

Mutations in Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> cotransporter (NBC-1) cause proximal renal tubular acidosis (pRTA) associated with ocular abnormalities. One pRTA patient had increased serum amylase, suggesting possible evidence of pancreatitis. To further delineate a link between NBC-1 inactivation and pancreatic dysfunction, immunohistochemical analysis was performed on rat and human pancreas using antibodies against kidney-type (kNBC-1) and pancreatic-type (pNBC-1) transporters. In rat pancreas, the anti-pNBC-1 antibody labeled acinar cells and both apical and basolateral membranes of medium and large duct cells. In human pancreas, on the other hand, the anti-pNBC-1 antibody did not label acinar cells, although it did label the basolateral membranes of the entire duct system. The labeling by anti-kNBC-1 antibody was detected in only a limited number of rat pancreatic duct cells. To examine the effects of pRTA-related mutations, R342S and R554H, on pNBC-1 function, we performed functional analysis and found that both mutants had reduced transport activities compared with the wild-type pNBC-1. These results indicate that pNBC-1 is the predominant variant that mediates basolateral HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> uptake into duct cells in both rat and human pancreas. The loss of pNBC-1 function is predicted to have significant impact on overall ductal HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> secretion, which could potentially lead to pancreatic dysfunction.

Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> cotransporter; pRTA; pancreatic duct cells; pancreatitis


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