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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 11 4178-4184
Copyright © 1999 by The Endocrine Society


Original Studies

Analysis of Human Sodium Iodide Symporter Immunoreactivity in Human Exocrine Glands1

C. Spitzweg, W. Joba, K. Schriever, J. R. Goellner, J. C. Morris and A. E. Heufelder

Departments of Endocrinology (C.S., J.C.M.) and Pathology (J.R.G.), Mayo Clinic, Rochester, Minnesota 55905; and the Division of Gastroenterology, Endocrinology, and Metabolism, Zentrum für Innere Medizin, Philipps-University, D-35033 Marburg, Germany

Address all correspondence and requests for reprints to: Dr. Christine Spitzweg, Mayo Clinic, Endocrine Research Unit, Guggenheim 625, 200 First Street SW, Rochester, Minnesota 55905. E-mail: spitzweg.christine{at}mayo.edu

The human sodium iodide symporter (hNIS) is an intrinsic transmembrane protein that mediates the active transport of iodide across the basolateral membrane of thyroid follicular cells. In addition to normally functioning thyroid tissue, various extrathyroidal tissues, including salivary gland, lacrimal gland, gastric mucosa, choroid plexus, and lactating mammary gland, have been demonstrated to accumulate iodide. After cloning and molecular characterization of the sodium iodide symporter, expression of hNIS messenger ribonucleic acid has been detected in a broad range of extrathyroidal tissues using Northern blot analysis and RT-PCR. In this study we used both monoclonal and polyclonal antibodies directed against different portions of hNIS protein together with a highly sensitive immunostaining technique to assess hNIS protein expression in tissue sections derived from normal human salivary and lacrimal glands, pancreas, as well as gastric and colonic mucosa. Immunohistochemical analysis of normal human salivary and lacrimal glands revealed marked hNIS immunoreactivity in ductal cells and less intense staining of acinar cells. Further, immunostaining of gastric and colonic mucosa showed marked hNIS immunoreactivity confined to chief and parietal cells in gastric mucosa and to epithelial cells lining mucosal crypts in colonic mucosa. In normal human pancreas, hNIS immunoreactivity was located in ductal cells, exocrine parenchymal cells, and Langerhans islet cells. In conclusion, our study demonstrates the expression of hNIS protein by several human exocrine glands, suggesting that iodide transport in these glands is a specific property conferred by the expression of hNIS protein, which may serve important functions by concentrating iodine in glandular secretions.




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