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Pendrin does not increase sulfate uptake in mammalian COS-7 cells
F Bogazzi1, L Bartalena, F Raggi
1Dipartimento di Endocrinologia e Metabolismo, Ortopedia e Traumatologia, Medicina del Lavoro, University of Pisa, Italy. fbogazzi@hotmail.com
Journal of Endocrinological Investigation
|May 10, 2000
Summary
Pendred's syndrome, a common cause of congenital deafness, is linked to the PDS gene. Research indicates pendrin (PDS) is not a sulfate transporter, contrary to previous hypotheses.
Area of Science:
- Genetics
- Endocrinology
- Otolaryngology
Background:
- Pendred's syndrome is a frequent genetic cause of congenital deafness, affecting ~10% of hereditary hearing loss.
- Mutations in the pendrin (PDS) gene are implicated in Pendred's syndrome.
- Pendrin's homology to known transporters led to the hypothesis that it functions in sulfate transport.
Purpose of the Study:
- To investigate whether pendrin (PDS) functions as a sulfate transporter.
- To elucidate the role of pendrin in thyroid and inner ear function.
Main Methods:
- Mammalian COS-7 cells were transiently transfected with PDS cDNA.
- Sulfate (35SO4) uptake was measured in transfected and mock-transfected cells over time.
- The effect of increasing PDS-plasmid concentrations on sulfate uptake was assessed.
Main Results:
- Sulfate uptake increased in a time-dependent manner in both PDS-transfected and mock-transfected cells.
- No significant difference in sulfate uptake was observed between PDS-transfected and mock-transfected cells.
- Increasing amounts of PDS-containing plasmid did not significantly enhance sulfate uptake.
Conclusions:
- The study provides evidence that pendrin (PDS) is not a sulfate transporter.
- Further functional studies are necessary to determine pendrin's precise role in thyroid pathophysiology and inner ear development.