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Articles in PresS, published online ahead of print November 20, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00166.2002
Submitted on April 11, 2002
Accepted on November 14, 2002
1 Internal Medicine, Tokyo University, Tokyo, Japan
2 Hemodialysis and Apheresis, Tokyo University, Tokyo, Japan
3 Pharmacology and Toxicology, Kyorin University, Tokyo, Japan
4 Anatomy, Kyorin University, Tokyo, Japan
5 Pediatrics, Tokyo University, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: georgeseki-tky{at}umin.ac.jp.
Mutations in Na+ -HCO3- 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, but did label the basolateral membranes of 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 to the wild-type pNBC-1. These results indicate that pNBC-1 is the predominant variant that mediates basolateral HCO3- 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 HCO3- secretion, which potentially could lead to pancreatic dysfunction.
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