Evidence map›Paper›PMID 25573755›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

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

Weiling Wang, Fei Li, Yi Sun, Lei Lei, Hong Zhou, Tianluo Lei, Yin Xia, A S Verkman, Baoxue Yang

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. MicroRNAs and Sepsis-Induced Cardiac Dysfunction: A Systematic Review.International journal of molecular sciences · 2020
    Pooled it
  3. Broadening horizons: Pathogenesis and therapeutics of renal ciliopathies.Journal of cell communication and signaling · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Aquaporins in Urinary System.Advances in experimental medicine and biology · 2023
    Article
  11. Review
  12. Article
  13. From Channels to Canonical Wnt Signaling: A Pathological Perspective.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 3 countries.

Weiling Wang*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Fei Li*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Yi Sun*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Lei Lei*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Hong Zhou*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Tianluo Lei*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Yin Xia*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
A S Verkman*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA.
Baoxue Yang*Department of Pharmacology, School of Basic Medical Sciences, Peking University, and State Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China; and Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California USA baoxue@bjmu.edu.cn.
Ministry of Education · ROState Key Laboratory of Natural and Biomimetic DrugsChinese University of Hong Kong · CNPeking University · CNUniversity of California, San Francisco · US

Funding

MECHANISMS OF WATER TRANSPORT IN RENAL EPITHELIAR37DK035124 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VERKMAN, ALAN S · 1999 to 2008
$4.2M
WATER AND NON-ELECTROLYTE TRANSPORT IN RENAL VESICLESR01DK035124 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VERKMAN, ALAN S · 1986 to 2014
$1.4M
NIDDK NIH HHS DK35124NIDDK NIH HHS R01 DK035124NIDDK NIH HHS R37 DK035124
6 · The paper itself

Abstract

Water channel aquaporin-1 (AQP1) is expressed at epithelial cell plasma membranes in renal proximal tubules and thin descending limb of Henle. Recently, AQP1 was reported to interact with β-catenin. Here we investigated the relationship between AQP1 and Wnt signaling in in vitro and in vivo models of autosomal dominant polycystic kidney disease (PKD). AQP1 overexpression decreased β-catenin and cyclinD1 expression, suggesting down-regulation of Wnt signaling, and coimmunoprecipitation showed AQP1 interaction with β-catenin, glycogen synthase kinase 3β, LRP6, and Axin1. AQP1 inhibited cyst development and promoted branching in matrix-grown MDCK cells. In embryonic kidney cultures, AQP1 deletion increased cyst development by up to ∼ 40%. Kidney size and cyst number were significantly greater in AQP1-null PKD mice than in AQP1-expressing PKD mice, with the difference mainly attributed to a greater number of proximal tubule cysts. Biochemical analysis revealed decreased β-catenin phosphorylation and increased β-catenin expression in AQP1-null PKD mice, suggesting enhanced Wnt signaling. These results implicate AQP1 as a novel determinant in renal cyst development that may involve inhibition of Wnt signaling by an AQP1-macromolecular signaling complex.

Indexed as

Wnt Signaling PathwayAnimalsAquaporin 1beta CateninCell AdhesionCell ProliferationCells, CulturedDisease Models, AnimalDogsKidneyMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalMultiprotein ComplexesPolycystic Kidney, Autosomal DominantAqp1 protein, mouseAquaporin 1beta CateninCTNNB1 protein, mouseMultiprotein ComplexesADPKDdestruction complexMDCKwater channel

Identifiers

PMID25573755
PMCPMC4396615
OpenAlexW2022210570

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.