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Expression of PDS/Pds, the Pendred syndrome gene, in endometrium
Koichi Suzuki1, Ines E Royaux, Lorraine A Everett
1Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan. koichis@nih.go.jp
Insights
The Pendred syndrome gene (PDS) and its protein pendrin are expressed in the human endometrium. Pendrin
Area of Science:
- Endocrinology
- Genetics
- Molecular Biology
Background:
- The Pendred syndrome gene (PDS) encodes the protein pendrin, crucial for iodide transport in the thyroid and inner ear development.
- PDS/pendrin expression is also documented in the kidney and placenta.
- The role of PDS/pendrin in the endometrium was previously uncharacterized.
Purpose of the Study:
- To investigate the expression and localization of PDS/pendrin in the human endometrium.
- To compare PDS/pendrin expression patterns in rats and humans.
- To explore the potential function of pendrin in endometrial physiology.
Main Methods:
- Analysis of PDS/pendrin mRNA and protein expression in human and rat endometrium.
- Immunohistochemical localization of pendrin within endometrial tissue.
- Comparison of expression levels across different tissues and species.
Main Results:
- PDS/pendrin is expressed in the human endometrium, with RNA levels higher in rat endometrium and kidney than thyroid.
- In human endometrium, pendrin translocates from the basal to apical surface during the menstrual cycle.
- Expression patterns differ between rats and humans, with higher endometrial PDS RNA in rats.
Conclusions:
- Pendrin expression and dynamic localization in the endometrium suggest a role in cationic ion transport.
- This function may be essential for maintaining endometrial physiological function.
- The absence of endometrial abnormalities in Pendred syndrome patients implies compensatory mechanisms in the uterus.
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.