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Wagner
The emerging role of pendrin in renal chloride reabsorption.
Wagner CA.
Am J Physiol Renal Physiol. 2007 Mar;292(3):F912-3. Epub 2006 Dec 12.
"The establishment of pendrin as a pathway for transcellular chloride absorption in the connecting tubule and cortical collecting segment certainly emphasizes the role of intercalated cells not only in acid-base transport but also in the control of electrolyte homeostasis and ultimately blood pressure.
"Many questions remain open: what is the relative importance of pendrin as transcellular transport pathway in relation to paracellular pathways under various conditions; how are pendrin abundance and activity regulated and coordinated with ENaC activity; what is the chloride sensor that mediates pendrin upregulation during chloride depletion; and is pendrin involved in the development of hypertension?"
Regulation of the expression of the Cl-/anion exchanger pendrin in mouse kidney by acid-base status.
Wagner CA, Finberg KE, Stehberger PA, Lifton RP, Giebisch GH, Aronson PS, Geibel JP.
Kidney Int. 2002 Dec;62(6):2109-17.
"BACKGROUND: Pendrin belongs to a superfamily of Cl-/anion exchangers and is expressed in the inner ear, the thyroid gland, and the kidney. In humans, mutations in pendrin cause Pendred syndrome characterized by sensorineural deafness and goiter. Recently pendrin has been localized to the apical side of non-type A intercalated cells of the cortical collecting duct, and reduced bicarbonate secretion was demonstrated in a pendrin knockout mouse model. To investigate a possible role of pendrin in modulating acid-base transport in the cortical collecting duct, we examined the regulation of expression of pendrin by acid-base status in mouse kidney.
METHODS: Mice were treated orally either with an acid or bicarbonate load (0.28 mol/L NH4Cl or NaHCO3) or received a K+-deficient diet for one week. Immunohistochemistry and Western blotting was performed.
RESULTS: Acid-loading caused a reduction in pendrin protein expression levels within one day and decreased expression to 23% of control levels after one week. Concomitantly, pendrin protein was shifted from the apical membrane to the cytosol, and the relative abundance of pendrin positive cells declined. Similarly, in chronic K+-depletion, known to elicit a metabolic alkalosis, pendrin protein levels decreased and pendrin expression was shifted to an intracellular pool with the relative number of pendrin positive cells reduced. In contrast, following oral bicarbonate loading pendrin was found exclusively in the apical membrane and the relative number of pendrin positive cells increased.
CONCLUSIONS: These results are in agreement with a potential role of pendrin in bicarbonate secretion and regulation of acid-base transport in the cortical collecting duct."