Evidence map›Paper›PMID 32442241›Full record

ArticleThe Journal of general physiology2020

Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner.

Morag K Mansley, Christian Niklas, Regina Nacken, Kathrin Mandery, Hartmut Glaeser, Martin F Fromm, Christoph Korbmacher, Marko Bertog

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Association of Urinary PGE2 with Plasma Potassium in Patients with CKD and the General Population.Clinical journal of the American Society of Nephrology : CJASN · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. NaHypertension (Dallas, Tex. : 1979) · 2022
    Article
  13. 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

8 authors at 1 institution in 1 country.

Morag K MansleyInstitute of Cellular and Molecular Physiology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Christian NiklasInstitute of Cellular and Molecular Physiology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Regina NackenInstitute of Cellular and Molecular Physiology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Kathrin ManderyInstitute of Experimental and Clinical Pharmacology and Toxicology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Hartmut GlaeserInstitute of Experimental and Clinical Pharmacology and Toxicology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Martin F FrommInstitute of Experimental and Clinical Pharmacology and Toxicology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Christoph KorbmacherInstitute of Cellular and Molecular Physiology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Marko BertogInstitute of Cellular and Molecular Physiology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostaglandin E2 (PGE2) is the most abundant prostanoid in the kidney, affecting a wide range of renal functions. Conflicting data have been reported regarding the effects of PGE2 on tubular water and ion transport. The amiloride-sensitive epithelial sodium channel (ENaC) is rate limiting for transepithelial sodium transport in the aldosterone-sensitive distal nephron. The aim of the present study was to explore a potential role of PGE2 in regulating ENaC in cortical collecting duct (CCD) cells. Short-circuit current (ISC) measurements were performed using the murine mCCDcl1 cell line known to express characteristic properties of CCD principal cells and to be responsive to physiological concentrations of aldosterone and vasopressin. PGE2 stimulated amiloride-sensitive ISC via basolateral prostaglandin E receptors type 4 (EP4) with an EC50 of ∼7.1 nM. The rapid stimulatory effect of PGE2 on ISC resembled that of vasopressin. A maximum response was reached within minutes, coinciding with an increased abundance of β-ENaC at the apical plasma membrane and elevated cytosolic cAMP levels. The effects of PGE2 and vasopressin were nonadditive, indicating similar signaling cascades. Exposing mCCDcl1 cells to aldosterone caused a much slower (∼2 h) increase of the amiloride-sensitive ISC. Interestingly, the rapid effect of PGE2 was preserved even after aldosterone stimulation. Furthermore, application of arachidonic acid also increased the amiloride-sensitive ISC involving basolateral EP4 receptors. Exposure to arachidonic acid resulted in elevated PGE2 in the basolateral medium in a cyclooxygenase 1 (COX-1)-dependent manner. These data suggest that in the cortical collecting duct, locally produced and secreted PGE2 can stimulate ENaC-mediated transepithelial sodium transport.

Indexed as

Epithelial Sodium ChannelsKidney Tubules, CollectingAnimalsCell LineDinoprostoneEpithelial Sodium Channel AgonistsIon TransportMiceDinoprostoneEpithelial Sodium Channel AgonistsEpithelial Sodium Channels

Identifiers

PMID32442241
PMCPMC7398144
OpenAlexW3027660038

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.