Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan (K.S.); Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland (I.E.R., L.A.E., E.D.G.); Department of Internal Medicine, Tottori University School of Medicine, Yonago, Japan (A.M-A.); Laboratory of Molecular Endocrinology, MedStar Research Institute, Washington Hospital Center, Washington, D.C. (K.S., S.S.); Laboratory of Cell Biology, Department of Regulation Biology, Saitama University, Urawa, Japan (K.N., T.S.); Department of Pathology, Yamanashi Medical University, Tamaho, Japan (R.K.); Department of Pathology, Saga Medical School, Saga, Japan (S.T.); and Ohio University School of Osteopathic Medicine and Edison Biotechnology Institute, Athens, Ohio (L.D.K.)
Abstract
Expression of the Pendred syndrome gene (PDS/Pds) is thought to be responsible for the iodide transport in the thyroid as well as the formation and function of the inner ear. Its mRNA is also expressed in the kidney and placenta. We report here that PDS and its encoded protein (pendrin) are also expressed in the endometrium. The RNA levels of rat PDS in the endometrium and kidney were much higher than those of the thyroid, opposite of the pattern of RNA expression in humans. In human endometrium, pendrin localization changed from the basal to apical surfaces of the epithelium during progression of the menstrual cycle. This suggests a possible role for pendrin in cationic ion transport required to maintain the physiological function of the endometrium. Since there is no evidence of endometrial abnormalities in patients with Pendred syndrome, it suggests the existence of a compensatory mechanisms for pendrins function in the uterus.