title: Sgk1 sensitive pendrin expression in murine platelets.
abstract: BACKGROUND
  The anion exchanger pendrin (SLC26A4) 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. SLC26A4 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 SGK1.
  
  
  METHODS
  The present study utilized i) quantitative reverse transcription polymerase chain reaction (RT-qPCR) to quantify the transcript levels of Slc26a4 as compared to Gapdh and ii) western blotting to assess Slc26a4 protein abundance in murine platelets from gene-targeted mice lacking Sgk1 (sgk1(-/-)) and respective wild type animals (sgk1(+/+)) treated without or with a subcutaneous injection of 2.5 mg DOCA for 3 h, or in sgk1(+/+) platelets with or without in vitro treatment for 1 h with 10 µg/ml DOCA.
  
  
  RESULTS
  Slc26a4 was expressed in platelets, and in vitro DOCA treatment increased Slc26a4 mRNA levels in platelets isolated from sgk1(+/+) mice. Moreover, in vivo DOCA treatment significantly up-regulated Slc26a4 mRNA levels in platelets isolated from sgk1(+/+) but not sgk1(-/-) mice. An increase in Sgk1 mRNA levels paralleled that of Slc26a4 mRNA levels in platelets of sgk1(+/+) mice. In addition, DOCA treatment further increased Slc26a4 protein abundance in platelets isolated from sgk1(+/+) mice.
  
  
  CONCLUSIONS
  Pendrin is expressed in platelets and is presumably regulated by SGK1 and mineralocorticoids.
authors.affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.
authors.forename: Lisann
authors.initials: L
authors.lastname: Pelzl
authors.forename: Hajar
authors.initials: H
authors.lastname: Fakhri
authors.forename: Anja T
authors.initials: AT
authors.lastname: Umbach
authors.forename: Meinrad
authors.initials: M
authors.lastname: Gawaz
authors.forename: Markus
authors.initials: M
authors.lastname: Paulmichl
authors.forename: Florian
authors.initials: F
authors.lastname: Lang
mesh_terms: D000818:Animals; D027321:Anion Transport Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D064791:Desoxycorticosterone Acetate / Q000494:pharmacology; D007758:Ear, Inner / Q000002:abnormalities / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006044:Goiter, Nodular / Q000235:genetics* / Q000473:pathology; D006319:Hearing Loss, Sensorineural / Q000235:genetics* / Q000473:pathology; D017874:Immediate-Early Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D051379:Mice; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D000076988:Sulfate Transporters; D013961:Thyroid Gland / Q000378:metabolism; D000099184:Serum-Glucocorticoid Regulated Kinases
chemical_list: D027321:Anion Transport Proteins; D064791:Desoxycorticosterone Acetate; D017874:Immediate-Early Proteins; D017346:Protein Serine-Threonine Kinases; D000076988:Sulfate Transporters; D000099184:Serum-Glucocorticoid Regulated Kinases; C494849:Slc26a4 protein, mouse