Evidence map›Paper›PMID 23977387›Full record

ArticlePloS one2013

TRPP2 and TRPV4 form an EGF-activated calcium permeable channel at the apical membrane of renal collecting duct cells.

Zhi-Ren Zhang, Wen-Feng Chu, Binlin Song, Monika Gooz, Jia-Ning Zhang, Chang-Jiang Yu, Shuai Jiang, Aleksander Baldys, Pal Gooz, Stacy Steele and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

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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

14 authors at 4 institutions in 3 countries.

Zhi-Ren ZhangDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States of America.
Wen-Feng Chu
Binlin Song
Monika Gooz
Jia-Ning Zhang
Chang-Jiang Yu
Shuai Jiang
Aleksander Baldys
Pal Gooz
Stacy Steele
Grzegorz Owsianik
Bernd Nilius
Peter Komlosi
P Darwin Bell
Medical University of South Carolina · USHarbin Medical University · CNKU Leuven · BERalph H. Johnson VA Medical Center · US

Funding

UAB Recessive PKD Research and Translational Core CenterP30DK074038 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 2005 to 2019
$16.6M
CELLULAR MECHANISMS--TUBULOGLOMERULAR FEEDBACK SYSTEMR01DK032032 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BELL, PHILLIP DARWIN · 1986 to 2009
$2.5M
NIDDK NIH HHS DK074038NIDDK NIH HHS P30 DK074038NIDDK NIH HHS R01 DK032032PHS HHS NIH/NIDDK RO1 DK32032
6 · The paper itself

Abstract

objectiveRegulation of apical calcium entry is important for the function of principal cells of the collecting duct. However, the molecular identity and the regulators of the transporter/channel, which is responsible for apical calcium entry and what factors regulate the calcium conduction remain unclear. METHODS AND

resultsWe report that endogenous TRPP2 and TRPV4 assemble to form a 23-pS divalent cation-permeable non-selective ion channel at the apical membrane of renal principal cells of the collecting duct. TRPP2\TRPV4 channel complex was identified by patch-clamp, immunofluorescence and co-immunprecipitation studies in both principal cells that either possess normal cilia (cilia (+)) or in which cilia are absent (cilia (-)). This channel has distinct biophysical and pharmacological and regulatory profiles compared to either TRPP2 or TRPV4 channels. The rate of occurrence detected by patch clamp was higher in cilia (-) compared to cilia (+) cells. In addition, shRNA knockdown of TRPP2 increased the prevalence of TRPV4 channel activity while knockdown of TRPV4 resulted in TRPP2 activity and knockdown of both proteins vastly decreased the 23-pS channel activity. Epidermal growth factor (EGF) stimulated TRPP2\TRPV4 channel through the EGF receptor (EGFR) tyrosine kinase-dependent signaling. With loss of cilia, apical EGF treatment resulted in 64-fold increase in channel activity in cilia (-) but not cilia (+) cells. In addition EGF increased cell proliferation in cilia (-) cell that was dependent upon TRPP2\TRPV4 channel mediated increase in intracellular calcium.

conclusionWe conclude that in the absence of cilia, an EGF activated TRPP2\TRPV4 channel may play an important role in increased cell proliferation and cystogenesis.

Indexed as

AnimalsCalciumCalcium Channel AgonistsCations, DivalentCell Membrane PermeabilityCell PolarityCell ProliferationCiliaEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFluorescent Antibody TechniqueGene SilencingImmunoprecipitationIon Channel GatingKidney Tubules, CollectingCalciumCalcium Channel AgonistsCations, DivalentEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesTRPP Cation ChannelsTrpv4 protein, mouseTRPV Cation Channels

Identifiers

PMID23977387
PMCPMC3745395
OpenAlexW2000447670

What OpenQuestion holds

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LicenceCC BY
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.