Literature DB >> 12217866

Immunocytochemical localization of pendrin in intercalated cell subtypes in rat and mouse kidney.

Young-Hee Kim1, Tae-Hwan Kwon, Sebastian Frische, Jin Kim, C Craig Tisher, Kirsten M Madsen, Søren Nielsen.   

Abstract

Recent studies have demonstrated that a novel anion exchanger, pendrin, is expressed in the apical domain of type B intercalated cells in the mammalian collecting duct. The purpose of this study was 1) to determine the expression and distribution of pendrin along the collecting duct and connecting tubule of mouse and rat kidney and establish whether pendrin is expressed in the non-A-non-B intercalated cells and 2) to determine the intracellular localization of pendrin in the different populations of intercalated cells by immunoelectron microscopy. A peptide-derived affinity-purified antibody was generated that specifically recognized pendrin in immunoblots of rat and mouse kidney. Immunohistochemistry and confocal laser scanning microscopy demonstrated the presence of pendrin in apical domains of all type B intercalated cells in mouse and rat connecting tubule and collecting duct. In addition, strong pendrin immunostaining was observed in non-A-non-B intercalated cells. There was no labeling of type A intercalated cells. Immunoelectron microscopy demonstrated that pendrin was located in the apical plasma membrane and intracellular vesicles of both type B intercalated cells and non-A-non-B cells; the latter was identified by the presence of H(+)-ATPase in the apical plasma membrane. The results of this study demonstrate that both pendrin and H(+)-ATPase are expressed in the apical plasma membrane of non-A-non-B intercalated cells, suggesting that these cells are capable of both HCO and proton secretion. Furthermore, the presence of pendrin in both the apical plasma membrane and the apical intracellular vesicles of type B and non-A-non-B intercalated cells suggests that HCO secretion may be regulated by trafficking of pendrin between the two membrane compartments.

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Year:  2002        PMID: 12217866     DOI: 10.1152/ajprenal.00037.2002

Source DB:  PubMed          Journal:  Am J Physiol Renal Physiol        ISSN: 1522-1466


  72 in total

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3.  Luminal flow modulates H+-ATPase activity in the cortical collecting duct (CCD).

Authors:  Wen Liu; Núria M Pastor-Soler; Carlos Schreck; Beth Zavilowitz; Thomas R Kleyman; Lisa M Satlin
Journal:  Am J Physiol Renal Physiol       Date:  2011-09-28

4.  Targeting of the hair cell proteins cadherin 23, harmonin, myosin XVa, espin, and prestin in an epithelial cell model.

Authors:  Lili Zheng; Jing Zheng; Donna S Whitlon; Jaime García-Añoveros; James R Bartles
Journal:  J Neurosci       Date:  2010-05-26       Impact factor: 6.167

Review 5.  Maintaining K+ balance on the low-Na+, high-K+ diet.

Authors:  Ryan J Cornelius; Bangchen Wang; Jun Wang-France; Steven C Sansom
Journal:  Am J Physiol Renal Physiol       Date:  2016-01-06

Review 6.  An unexpected journey: conceptual evolution of mechanoregulated potassium transport in the distal nephron.

Authors:  Rolando Carrisoza-Gaytan; Marcelo D Carattino; Thomas R Kleyman; Lisa M Satlin
Journal:  Am J Physiol Cell Physiol       Date:  2015-12-02       Impact factor: 4.249

7.  Role of NKCC in BK channel-mediated net K⁺ secretion in the CCD.

Authors:  Wen Liu; Carlos Schreck; Richard A Coleman; James B Wade; Yubelka Hernandez; Beth Zavilowitz; Richard Warth; Thomas R Kleyman; Lisa M Satlin
Journal:  Am J Physiol Renal Physiol       Date:  2011-08-03

8.  Pendrin localizes to the adrenal medulla and modulates catecholamine release.

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Journal:  Am J Physiol Endocrinol Metab       Date:  2015-07-14       Impact factor: 4.310

9.  Role of pendrin in iodide balance: going with the flow.

Authors:  Young Hee Kim; Truyen D Pham; Wencui Zheng; Seongun Hong; Christine Baylis; Vladimir Pech; William H Beierwaltes; Donna B Farley; Lewis E Braverman; Jill W Verlander; Susan M Wall
Journal:  Am J Physiol Renal Physiol       Date:  2009-07-15

10.  Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure.

Authors:  Manoocher Soleimani; Sharon Barone; Jie Xu; Gary E Shull; Faraz Siddiqui; Kamyar Zahedi; Hassane Amlal
Journal:  Proc Natl Acad Sci U S A       Date:  2012-07-30       Impact factor: 11.205

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