Evidence map›Paper›PMID 17957381›Full record

ReviewPflugers Archiv : European journal of physiology2008

Calcium signaling in vasopressin-induced aquaporin-2 trafficking.

Lavanya Balasubramanian, James S K Sham, Kay-Pong Yip

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Aquaporin Modulation by Cations, a Review.Current issues in molecular biology · 2024
    Review
  4. TRPML1-Induced Lysosomal CaInternational journal of molecular sciences · 2023
    Article
  5. Updates and Perspectives on Aquaporin-2 and Water Balance Disorders.International journal of molecular sciences · 2021
    Review
  6. A peek into Epac physiology in the kidney.American journal of physiology. Renal physiology · 2019
    Article
  7. Urinary concentrating defect in mice lacking Epac1 or Epac2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus.Journal of the American Society of Nephrology : JASN · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Aquaporins in kidney pathophysiology.Nature reviews. Nephrology · 2010
    Review
  19. Article
  20. EPAC proteins transduce diverse cellular actions of cAMP.British journal of pharmacology · 2009
    Review
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

3 authors at 2 institutions in 1 country.

Lavanya BalasubramanianDepartment of Molecular Pharmacology and Physiology, College of Medicine, University of South Florida, Tampa, FL 33612, USA.
James S K Sham
Kay-Pong Yip
University of South Florida · USJohns Hopkins University · US

Funding

Local Calcium Signaling in Pulmonary ArteriesR01HL071835 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHAM, JAMES SK · 2003 to 2012
$3.4M
Regulation of aquaporin-2 trafficking in collecting ductR01DK060501 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI YIP, KAY-PONG DANIEL · 2003 to 2006
$730k
NHLBI NIH HHS R01 HL071835NIDDK NIH HHS DK-60501NIDDK NIH HHS R01 DK060501
6 · The paper itself

Abstract

It has been the general consensus that cAMP-mediated PKA-dependent phosphorylation of aquaporin-2 is the primary mechanism of vasopressin to regulate osmotic water permeability in kidney collecting duct. By using laser scanning confocal microscopy to monitor [Ca2+]i and apical exocytosis in individual cells of inner medullary collecting duct, we have demonstrated that vasopressin also triggers intracellular Ca2+ mobilization, which is coupled to apical exocytotic insertion of aquaporin-2. Vasopressin-induced Ca2+ mobilization is in the form of oscillations, which involves both intracellular Ca2+ release from ryanodine-gated Ca2+ stores and extracellular Ca2+ influx via capacitative calcium entry. Each individual cell operates as an independent calcium oscillator with time variance in frequency and amplitude. Vasopressin-induced Ca2+ mobilization is mediated by cAMP, but is independent of PKA. Exogenous cAMP analog (8-pCPT-2'-O-Me-cAMP), which activates Epac (exchange protein directly activated by cAMP), but not PKA, triggers Ca2+ mobilization and apical exocytosis. These observations suggest that activation of Epac by cAMP may also contribute to the action of vasopressin in regulating osmotic water permeability. There are multiple plausible candidates for downstream effectors of vasopressin-induced Ca2+ signal including calmodulin, myosin light chain kinase, calmodulin kinase II, and calcineurin. All of them have been implicated in the regulation of aquaporin-2 trafficking and/or water permeability.

Indexed as

AnimalsAquaporin 2CalciumCalcium SignalingCyclic AMP-Dependent Protein KinasesHumansVasopressinsAquaporin 2CalciumCyclic AMP-Dependent Protein KinasesVasopressins

Identifiers

PMID17957381
OpenAlexW1997144932

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.