Sgk1 sensitive pendrin expression in murine platelets.

[pendred syndrome]

The anion exchanger pendrin (SLC 26 A 4 ) is required for proper development of the inner ear , and contributes to iodide organification in thyroid glands as well as anion transport in various epithelia , such as airways and renal tubules . SLC 26 A 4 deficiency leads to Pendred syndrome , which is characterized by hearing loss with enlarged vestibular aqueducts and variable hypothyroidism and goiter . Pendrin expression in kidney , heart , lung and thyroid is up-regulated by the mineralocorticoid deoxycorticosterone (DOCA ). Platelets express anion exchangers but virtually nothing is known about the molecular identity and regulation of those carriers . Other carriers such as the Na (+)/H (+) exchanger are regulated by the mineralocorticoid-sensitive serum and glucocorticoid inducible kinase SGK 1 .T he present study utilized i ) quantitative reverse transcription polymerase chain reaction (RT-qPCR ) to quantify the transcript levels of Slc 26 a 4 as compared to Gapdh and ii ) western blotting to assess Slc 26 a 4 protein abundance in murine platelets from gene -targeted mice lacking Sgk 1 (sgk 1 (-/-)) and respective wild type animals (sgk 1 (+/+)) treated without or with a subcutaneous injection of 2 .5 mg DOCA for 3 h , or in sgk 1 (+/+) platelets with or without in vitro treatment for 1 h with 10 µg /ml DOCA .Slc 26 a 4 was expressed in platelets , and in vitro DOCA treatment increased Slc 26 a 4 mRNA levels in platelets isolated from sgk 1 (+/+) mice . Moreover , in vivo DOCA treatment significantly up-regulated Slc 26 a 4 mRNA levels in platelets isolated from sgk 1 (+/+) but not sgk 1 (-/-) mice . An increase in Sgk 1 mRNA levels paralleled that of Slc 26 a 4 mRNA levels in platelets of sgk 1 (+/+) mice . In addition , DOCA treatment further increased Slc 26 a 4 protein abundance in platelets isolated from sgk 1 (+/+) mice .Pendrin is expressed in platelets and is presumably regulated by SGK 1 and mineralocorticoids .