Evidence map›Paper›PMID 23097465›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Role of protein kinase C-α in hypertonicity-stimulated urea permeability in mouse inner medullary collecting ducts.

Yanhua Wang, Janet D Klein, Otto Froehlich, Jeff M Sands

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Mammalian urine concentration: a review of renal medullary architecture and membrane transporters.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2018
    Review
  3. Article
  4. Article
  5. Urea transport and clinical potential of urearetics.Current opinion in nephrology and hypertension · 2016
    Review
  6. Article
  7. Review
  8. Article
  9. Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

4 authors at 1 institution in 1 country.

Yanhua WangEmory Univ. School of Medicine, Renal Division, Atlanta, GA 30322, USA. ywang68@emory.edu
Janet D Klein
Otto Froehlich
Jeff M Sands
Emory University · US

Funding

Regulation of Renal Inner Medullary FunctionR01DK041707 · NIDDK · EMORY UNIVERSITY · PI SANDS, JEFF M · 1996 to 2017
$4.3M
Regulation of Urea Transport by PKC-alphaR01DK089828 · NIDDK · EMORY UNIVERSITY · PI SANDS, JEFF M · 2011 to 2014
$1.5M
Novel Mouse Models for the Study of Urea TransportersR21DK091147 · NIDDK · EMORY UNIVERSITY · PI SANDS, JEFF M · 2011 to 2012
$233k
NIDDK NIH HHS R01 DK041707NIDDK NIH HHS R01 DK089828NIDDK NIH HHS R01-DK41707NIDDK NIH HHS R01-DK89828NIDDK NIH HHS R21 DK091147NIDDK NIH HHS R21-DK91147
6 · The paper itself

Abstract

The kidney's ability to concentrate urine is vitally important to our quality of life. In the hypertonic environment of the kidney, urea transporters must be regulated to optimize function. We previously showed that hypertonicity increases urea permeability and that the protein kinase C (PKC) blockers chelerythrine and rottlerin decreased hypertonicity-stimulated urea permeability in rat inner medullary collecting ducts (IMCDs). Because PKCα knockout (PKCα(-/-)) mice have a urine-concentrating defect, we tested the effect of hypertonicity on urea permeability in isolated perfused mouse IMCDs. Increasing the osmolality of perfusate and bath from 290 to 690 mosmol/kgH(2)O did not change urea permeability in PKCα(-/-) mice but significantly increased urea permeability in wild-type mice. To determine whether the response to protein kinase A was also missing in IMCDs of PKCα(-/-) mice, tubules were treated with vasopressin and subsequently with the PKC stimulator phorbol dibutyrate (PDBu). Vasopressin stimulated urea permeability in PKCα(-/-) mice. Like vasopressin, forskolin stimulated urea permeability in PKCα(-/-) mice. We previously showed that, in rats, vasopressin and PDBu have additive stimulatory effects on urea permeability. In contrast, in PKCα(-/-) mice, PDBu did not further increase vasopressin-stimulated urea permeability. Western blot analysis showed that expression of the UT-A1 urea transporter in IMCDs was increased in response to vasopressin in wild-type mice as well as PKCα(-/-) mice. Hypertonicity increased UT-A1 phosphorylation in wild-type mice but not in PKCα(-/-) mice. We conclude that PKCα mediates hypertonicity-stimulated urea transport but is not necessary for vasopressin stimulation of urea permeability in mouse IMCDs.

Indexed as

AnimalsBiological TransportColforsinKidney MedullaKidney Tubules, CollectingMiceMice, KnockoutPermeabilityPhorbol 12,13-DibutyrateProtein Kinase C-alphaSaline Solution, HypertonicUreaVasopressinsColforsinPhorbol 12,13-DibutyrateProtein Kinase C-alphaSaline Solution, HypertonicUreaVasopressins

Identifiers

PMID23097465
PMCPMC3543629
OpenAlexW2004573417

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.