Evidence map›Paper›PMID 26309024›Full record

ArticlePloS one2015

Epithelial Sodium Channel-Mediated Sodium Transport Is Not Dependent on the Membrane-Bound Serine Protease CAP2/Tmprss4.

Anna Keppner, Ditte Andreasen, Anne-Marie Mérillat, Julie Bapst, Camille Ansermet, Qing Wang, Marc Maillard, Sumedha Malsure, Antoine Nobile, Edith Hummler

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022
    Review
  9. Targeting Crucial Host Factors of SARS-CoV-2.ACS infectious diseases · 2020
    Review
  10. Article
  11. Review
  12. Article
  13. The epithelial NaPflugers Archiv : European journal of physiology · 2019
    Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. 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

10 authors at 2 institutions in 1 country.

Anna KeppnerDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
Ditte AndreasenDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
Anne-Marie MérillatDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
Julie BapstDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
Camille AnsermetDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
Qing WangDepartment of Medicine/Division of Nephrology and Hypertension, Lausanne University Hospital (CHUV), Lausanne, Switzerland; Department of Medicine/Physiology, University of Fribourg, Fribourg, Switzerland.
Marc MaillardDepartment of Medicine/Division of Nephrology and Hypertension, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Sumedha MalsureDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
Antoine NobileInstitut Universitaire de Pathologie, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Edith HummlerDepartment of Pharmacology & Toxicology, University of Lausanne, Lausanne, Switzerland.
University of Lausanne · CHUniversity Hospital of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The membrane-bound serine protease CAP2/Tmprss4 has been previously identified in vitro as a positive regulator of the epithelial sodium channel (ENaC). To study its in vivo implication in ENaC-mediated sodium absorption, we generated a knockout mouse model for CAP2/Tmprss4. Mice deficient in CAP2/Tmprss4 were viable, fertile, and did not show any obvious histological abnormalities. Unexpectedly, when challenged with sodium-deficient diet, these mice did not develop any impairment in renal sodium handling as evidenced by normal plasma and urinary sodium and potassium electrolytes, as well as normal aldosterone levels. Despite minor alterations in ENaC mRNA expression, we found no evidence for altered proteolytic cleavage of ENaC subunits. In consequence, ENaC activity, as monitored by the amiloride-sensitive rectal potential difference (ΔPD), was not altered even under dietary sodium restriction. In summary, ENaC-mediated sodium balance is not affected by lack of CAP2/Tmprss4 expression and thus, does not seem to directly control ENaC expression and activity in vivo.

Indexed as

Absorption, PhysicochemicalAnimalsBiological TransportCell MembraneEpithelial Sodium ChannelsGene Knockout TechniquesHomeostasisMembrane ProteinsMiceSerine EndopeptidasesSodiumEpithelial Sodium ChannelsMembrane ProteinsSerine EndopeptidasesSodiumTmprss4 protein, mouse

Identifiers

PMID26309024
PMCPMC4550455
OpenAlexW1948386551

What OpenQuestion holds

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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.