Literature DB >> 9069455

Expression and localization of the water channels in human autosomal dominant polycystic kidney disease.

M Hayashi1, Y Yamaji, T Monkawa, T Yoshida, H Tsuganezawa, H Sasamura, W Kitajima, S Sasaki, K Ishibashi, F Maurmo, T Saruta.   

Abstract

To characterize the cyst-lining cells in human autosomal dominant polycystic kidney disease (ADPKD), we performed immunohistological studies with specific antibodies against human aquaporin-2 (AQP-2, the vasopressin-regulated water channel) and aquaporin-3 (AQP-3), which are expressed only in collecting duct cells in the normal kidney. The polycystic kidney samples were obtained from 2 hemodialysis patient at uninephrectomy. Immunohistochemical studies revealed two types of staining of cyst-lining cells. Approximately 30% of all the cysts were simultaneously immunostained by both antibodies. Among these AQP-positive cysts, more than 90% of the cysts were intensely stained, with well-polarized localization of AQP-2 and AQP-3. In fewer than 10% of AQP-positive cysts, by contrast, immunostaining for AQP-2 and AQP-3 was faint and no clearly polarized localization of the channels was observed. We examined the immunostaining in further detail by electron microscopy. Staining specific for AQP-2 was mainly observed in the apical membrane of cyst-lining cells. Moreover, staining specific for AQP-3 was observed in all of the AQP-2-positive cysts. It appeared unlikely that the variations in immunostaining observed under the light microscope had been induced by total disruption of water-channel polarity. The present study suggests that about 30% of the cysts in our cases of ADPKD were derived from the collecting duct cells and that the cyst-lining cells were well differentiated in terms of AQP expression.

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Year:  1997        PMID: 9069455     DOI: 10.1159/000189556

Source DB:  PubMed          Journal:  Nephron        ISSN: 1660-8151            Impact factor:   2.847


  4 in total

Review 1.  Vasopressin and disruption of calcium signalling in polycystic kidney disease.

Authors:  Fouad T Chebib; Caroline R Sussman; Xiaofang Wang; Peter C Harris; Vicente E Torres
Journal:  Nat Rev Nephrol       Date:  2015-04-14       Impact factor: 28.314

2.  Inactivation of Pkd1 in principal cells causes a more severe cystic kidney disease than in intercalated cells.

Authors:  Kalani L Raphael; Kevin A Strait; Peter K Stricklett; R Lance Miller; Raoul D Nelson; Klaus B Piontek; Gregory G Germino; Donald E Kohan
Journal:  Kidney Int       Date:  2009-01-14       Impact factor: 10.612

3.  Calmodulin-sensitive adenylyl cyclases mediate AVP-dependent cAMP production and Cl- secretion by human autosomal dominant polycystic kidney cells.

Authors:  Cibele S Pinto; Gail A Reif; Emily Nivens; Corey White; Darren P Wallace
Journal:  Am J Physiol Renal Physiol       Date:  2012-09-05

4.  Aquaporin-3 deficiency slows cyst enlargement in experimental mouse models of autosomal dominant polycystic kidney disease.

Authors:  Weiling Wang; Xiaoqiang Geng; Lei Lei; Yingli Jia; Yingjie Li; Hong Zhou; Alan S Verkman; Baoxue Yang
Journal:  FASEB J       Date:  2019-02-15       Impact factor: 5.834

  4 in total

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