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Am J Physiol Endocrinol Metab (September 11, 2002). doi:10.1152/ajpendo.00383.2002
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Articles in PresS, published online ahead of print September 10, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00383.2002
Submitted on August 28, 2002
Accepted on September 4, 2002

Prolactin Regulation of the Pendrin Iodide Transporter in the Mammary Gland

James A. Rillema1* and Melissa A. Hill1

1 Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA

* To whom correspondence should be addressed. E-mail: jrillema{at}med.wayne.edu.

Iodide is an essential constituent of milk that is present in concentrations more than an order of magnitude higher than in the maternal plasma. Earlier, a sodium-iodide symporter was identified in the mammary gland; this transporter is presumed to take iodide from the maternal plasma into the alveolar epithelial cells of the mammary gland. We now report the existence of a second iodide transporter, pendrin, which is also essential for iodide accumulation in milk. Via western blotting methods, high levels of the transporter were detected in lactating tissues; lesser amounts were found in tissues from mid-pregnant and virgin mice. Prolactin, at physiological concentrations, stimulated the expression of the pendrin transporter in cultured mammary tissues taken from 12-14 day pregnant mice. The prolactin effect on iodide uptake into cultured mammary tissues was abolished by pendrin transport inhibitors including DIDS, furosemide and probenecid. These studies suggest that the prolactin stimulation of pendrin activity is an essential element in the prolactin stimulation of iodide uptake into milk.




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