Evidence map›Paper›PMID 23049542›Full record

ArticleExperimental diabetes research2012

Functional expression of TRPV4 channels in human collecting duct cells: implications for secondary hypertension in diabetic nephropathy.

Claire E Hills, Rosemary Bland, Paul E Squires

Open access · hybridAbstract read
In one paragraph

Article in Experimental diabetes research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. TRPV4: A Physio and Pathophysiologically Significant Ion Channel.International journal of molecular sciences · 2020
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Hydrogen peroxide-induced calcium influx in lung microvascular endothelial cells involves TRPV4.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  9. Flow regulation of endothelin-1 production in the inner medullary collecting duct.American journal of physiology. Renal physiology · 2015
    Article
  10. Review
  11. 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 1 institution in 1 country.

Claire E HillsSchool of Life Sciences, The University of Warwick, Coventry CV4 7AL, UK. c.hills@warwick.ac.uk
Rosemary Bland
Paul E Squires
University of Warwick · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Vanilloid subfamily of transient receptor potential (TRPV) ion channels has been widely implicated in detecting osmotic and mechanical stress. In the current study, we examine the functional expression of TRPV4 channels in cell volume regulation in cells of the human collecting duct.

methodsWestern blot analysis, siRNA knockdown, and microfluorimetry were used to assess the expression and function of TRPV4 in mediating Ca²⁺-dependent mechanical stimulation within a novel system of the human collecting duct (HCD).

resultsNative and siRNA knockdown of TRPV4 protein expression was confirmed by western blot analysis. Touch was used as a cell-directed surrogate for osmotic stress. Mechanical stimulation of HCD cells evoked a transient increase in [Ca²⁺](i) that was dependent upon thapsigargin-sensitive store release and Ca²⁺ influx. At 48 hrs, high glucose and mannitol (25 mM) reduced TRPV4 expression by 54% and 24%, respectively. Similar treatment doubled SGK1 expression. Touch-evoked changes were negated following TRPV4 knockdown.

conclusionOur data confirm expression of Ca²⁺-dependent TRPV4 channels in HCD cells and suggest that a loss of expression in response to high glucose attenuates the ability of the collecting duct to exhibit regulatory volume decreases, an effect that may contribute to the pathology of fluid and electrolyte imbalance as observed in diabetic nephropathy.

Indexed as

Down-RegulationCalcium SignalingCell Line, TransformedCell SizeClone CellsDiabetic NephropathiesGlucoseHumansHypertensionImmediate-Early ProteinsKidney Tubules, CollectingMannitolOsmotic PressurePhysical StimulationProtein Serine-Threonine KinasesRNA InterferenceGlucoseImmediate-Early ProteinsMannitolProtein Serine-Threonine KinasesRNA, MessengerRNA, Small InterferingSerum-Glucocorticoid Regulated KinasesTRPV4 protein, humanTRPV Cation Channels

Identifiers

PMID23049542
PMCPMC3461299
OpenAlexW2104502832

What OpenQuestion holds

Textmetadata
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.