Literature DB >> 7535000

Water channel expression in human ADPKD kidneys.

D R Bachinsky1, I Sabolic, D S Emmanouel, D M Jefferson, F A Carone, D Brown, R D Perrone.   

Abstract

Cyst enlargement in autosomal dominant polycystic kidney disease (ADPKD) results in part from the transport of solute and fluid into the lumen of the cyst. In proximal tubules and thin descending limbs of normal kidneys, the high transepithelial water permeability of these segments is due to the presence of the water channel protein, aquaporin-CHIP (AQP-CHIP, i.e., AQP-1). The collecting ducts of normal kidneys express another member of this gene family, the aquaporin collecting duct (AQP-CD, i.e., AQP-2). The expression and distribution of these two members of the aquaporin gene family were examined in ADPKD and normal human kidneys. In both tissues, Western blotting with the anti-AQP-CHIP antibody revealed a major 28-kDa band. By immunofluorescence, AQP-CHIP was present in proximal tubules and thin descending limbs of Henle of both normal and ADPKD kidneys. In the latter, AQP-CHIP was detected in the epithelia lining 71% of cysts. Many cysts were positive for the proximal tubule marker gp330 (44%). Some cysts expressing AQP-CHIP did not stain for gp330, suggesting a descending thin limb origin, and a few cysts were negative for both markers. In normal human kidney, Western blotting with the anti-AQP-CD antibody revealed a band at 28 kDa. AQP-CD was localized to collecting ducts and did not show colocalization with gp330 in normal human kidney. In ADPKD kidney, AQP-CD was expressed by only 8% of cysts. In summary, water channels, primarily AQP-CHIP, are expressed in epithelial cells lining cysts in approximately 80% of cysts in ADPKD kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1995        PMID: 7535000     DOI: 10.1152/ajprenal.1995.268.3.F398

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  5 in total

Review 1.  Cellular distribution of the aquaporins: a family of water channel proteins.

Authors:  D Brown; T Katsura; M Kawashima; A S Verkman; I Sabolic
Journal:  Histochem Cell Biol       Date:  1995-07       Impact factor: 4.304

2.  Aquaporin-1 retards renal cyst development in polycystic kidney disease by inhibition of Wnt signaling.

Authors:  Weiling Wang; Fei Li; Yi Sun; Lei Lei; Hong Zhou; Tianluo Lei; Yin Xia; A S Verkman; Baoxue Yang
Journal:  FASEB J       Date:  2015-01-08       Impact factor: 5.191

3.  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

4.  Effect of tolvaptan on renal handling of water and sodium, GFR and central hemodynamics in autosomal dominant polycystic kidney disease during inhibition of the nitric oxide system: a randomized, placebo-controlled, double blind, crossover study.

Authors:  Safa Al Therwani; My Emma Sofie Malmberg; Jeppe Bakkestroem Rosenbaek; Jesper Noergaard Bech; Erling Bjerregaard Pedersen
Journal:  BMC Nephrol       Date:  2017-08-15       Impact factor: 2.388

Review 5.  New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development.

Authors:  Ming Wu; Shengqiang Yu
Journal:  Kidney Dis (Basel)       Date:  2016-03-25
  5 in total

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