Evidence map›Paper›PMID 26578982›Full record

ArticleFrontiers in physiology2015

Dexamethasone increases aquaporin-2 protein expression in ex vivo inner medullary collecting duct suspensions.

Minguang Chen, Hui Cai, Janet D Klein, Oskar Laur, Guangping Chen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2015. 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
1.4field-weighted citation impact, top 19% 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. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Low aquaporin-2 excretion in the nephrotic syndrome: an escape from the vasopressin regulating effect.International journal of nephrology and renovascular disease · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. Nuclear Receptor Regulation of Aquaporin-2 in the Kidney.International journal of molecular sciences · 2016
    Review
  12. Modulation of kidney urea transporter UT-A3 activity by alpha2,6-sialylation.Pflugers Archiv : European journal of physiology · 2016
    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

5 authors at 2 institutions in 2 countries.

Minguang ChenDivision of Nephrology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Wenzhou, China ; Department of Physiology, Emory University School of Medicine Atlanta, GA, USA.
Hui CaiDepartment of Physiology, Emory University School of Medicine Atlanta, GA, USA ; Renal Division, Department of Medicine, Emory University School of Medicine Atlanta, GA, USA.
Janet D KleinDepartment of Physiology, Emory University School of Medicine Atlanta, GA, USA ; Renal Division, Department of Medicine, Emory University School of Medicine Atlanta, GA, USA.
Oskar LaurDepartment of Microbiology and Immunology, Emory University School of Medicine Atlanta, GA, USA.
Guangping ChenDepartment of Physiology, Emory University School of Medicine Atlanta, GA, USA ; Renal Division, Department of Medicine, Emory University School of Medicine Atlanta, GA, USA.
Emory University · USWenzhou Medical University · CN

Funding

Small Proteins and Renal Urea Transport RegulationR01DK087838 · NIDDK · EMORY UNIVERSITY · PI CHEN, GUANGPING · 2011 to 2015
$1.7M
Sodium Chloride Cotransporter Regulation by WNK KinaseK08DK068226 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI CAI, HUI · 2005 to 2010
$683k
BLRD VA I01 BX000994NIDDK NIH HHS K08 DK068226NIDDK NIH HHS R01 DK087838
6 · The paper itself

Abstract

Aquaporin-2 (AQP2) is the vasopressin-regulated water channel that controls renal water reabsorption and plays an important role in the maintenance of body water homeostasis. Excessive glucocorticoid as often seen in Cushing's syndrome causes water retention. However, whether and how glucocorticoid regulates AQP2 remains unclear. In this study, we examined the direct effect of dexamethasone on AQP2 protein expression and activity. Dexamethasone increased AQP2 protein abundance in rat inner medullary collecting duct (IMCD) suspensions. This was confirmed in HEK293 cells transfected with AQP2 cDNA. Cell surface protein biotinylation showed an increase of dexamethasone-induced cell membrane AQP2 expression and this effect was blocked by glucocorticoid receptor antagonist RU486. Functionally, dexamethasone treatment of oocytes injected with an AQP2 cRNA increased water transport activity as judged by cell rupture time in a hypo-osmotic solution (66 ± 13 s in dexamethasone vs. 101 ± 11 s in control, n = 15). We further found that dexamethasone treatment reduced AQP2 protein degradation, which could result in an increase of AQP2 protein. Interestingly, dexamethasone promoted cell membrane AQP2 moving to less buoyant lipid raft submicrodomains. Taken together, our data demonstrate that dexamethasone promotes AQP2 protein expression and increases water permeability mainly via inhibition of AQP2 protein degradation. The increase in AQP2 activity promotes water reabsorption, which may contribute to glucocorticoid-induced water retention and hypertension.

Indexed as

collecting ductsteroidurine concentrationvasopressinwater homeostasis

Identifiers

PMID26578982
PMCPMC4630297
OpenAlexW2190340234

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.