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 pendrin's function in the uterus.
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Authors | Koichi Suzuki, Ines E Royaux, Lorraine A Everett, Atsumi Mori-Aoki, Sayuri Suzuki, Kazuaki Nakamura, Takafumi Sakai, Ryohei Katoh, Shuji Toda, Eric D Green, Leonard D Kohn |
Journal | The Journal of clinical endocrinology and metabolism
(J Clin Endocrinol Metab)
Vol. 87
Issue 2
Pg. 938
(Feb 2002)
ISSN: 0021-972X [Print] United States |
PMID | 11836344
(Publication Type: Journal Article)
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Chemical References |
- Carrier Proteins
- Membrane Transport Proteins
- RNA, Messenger
- SLC26A4 protein, human
- Sulfate Transporters
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Topics |
- Animals
- Carrier Proteins
(genetics)
- Endometrium
(physiology)
- Epithelium
(metabolism)
- Female
- Gene Expression
- Humans
- Membrane Transport Proteins
- Menstrual Cycle
(metabolism)
- Mice
- RNA, Messenger
(metabolism)
- Rats
- Rats, Wistar
- Sulfate Transporters
- Tissue Distribution
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