Evidence map›Paper›PMID 27892464›Full record

ArticleNature communications2016

Wnt5a induces renal AQP2 expression by activating calcineurin signalling pathway.

Fumiaki Ando, Eisei Sohara, Tetsuji Morimoto, Naofumi Yui, Naohiro Nomura, Eriko Kikuchi, Daiei Takahashi, Takayasu Mori, Alain Vandewalle, Tatemitsu Rai and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Expression Regulation and Trafficking of Aquaporins.Advances in experimental medicine and biology · 2023
    Review
  10. Aquaporins in Urinary System.Advances in experimental medicine and biology · 2023
    Article
  11. Article
  12. Article
  13. Updates and Perspectives on Aquaporin-2 and Water Balance Disorders.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Rapid development of vasopressin resistance in dietary KAmerican journal of physiology. Renal physiology · 2021
    Article
  19. Article
  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

13 authors at 4 institutions in 3 countries.

Fumiaki AndoDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Eisei SoharaDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Tetsuji MorimotoDivision of Pediatrics, Tohoku Medical and Pharmaceutical University, Miyagi 983-8512, Japan.
Naofumi YuiDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Naohiro NomuraDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Eriko KikuchiDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Daiei TakahashiDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Takayasu MoriDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Alain VandewalleCentre de Recherche sur l'Inflammation (CRI), UMRS 1149, Université Denis Diderot-Paris 7, 75018 Paris, France.
Tatemitsu RaiDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Sei SasakiDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Yoshiaki KondoDepartment of Health Care Services Management, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Shinichi UchidaDepartment of Nephrology, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Tokyo Medical and Dental University · JPNihon University · JPTohoku Medical and Pharmaceutical University · JPUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heritable nephrogenic diabetes insipidus (NDI) is characterized by defective urine concentration mechanisms in the kidney, which are mainly caused by loss-of-function mutations in the vasopressin type 2 receptor. For the treatment of heritable NDI, novel strategies that bypass the defective vasopressin type 2 receptor are required to activate the aquaporin-2 (AQP2) water channel. Here we show that Wnt5a regulates AQP2 protein expression, phosphorylation and trafficking, suggesting that Wnt5a is an endogenous ligand that can regulate AQP2 without the activation of the classic vasopressin/cAMP signalling pathway. Wnt5a successfully increases the apical membrane localization of AQP2 and urine osmolality in an NDI mouse model. We also demonstrate that calcineurin is a key regulator of Wnt5a-induced AQP2 activation without affecting intracellular cAMP level and PKA activity. The importance of calcineurin is further confirmed with its activator, arachidonic acid, which shows vasopressin-like effects underlining that calcineurin activators may be potential therapeutic targets for heritable NDI.

Indexed as

Gene Expression RegulationSignal TransductionAnimalsAquaporin 2Arachidonic Acidbeta CateninCalcineurinCalciumCalcium SignalingCyclic AMPCyclic AMP-Dependent Protein KinasesDiabetes Insipidus, NephrogenicDisease Models, AnimalDishevelled ProteinsKidneyMaleAquaporin 2Arachidonic Acidbeta CateninCalcineurinCalciumCyclic AMPCyclic AMP-Dependent Protein KinasesDishevelled ProteinsPhosphoserineRNA, MessengerWaterWnt-5a ProteinWnt5a protein, mouse

Identifiers

PMID27892464
PMCPMC5133730
OpenAlexW2559469370

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.