Evidence map›Paper›PMID 31117121›Full record

ArticleInvestigative ophthalmology & visual science2019

Trabecular Meshwork TREK-1 Channels Function as Polymodal Integrators of Pressure and pH.

Oleg Yarishkin, Tam T T Phuong, David Križaj

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanobiology in the eye.npj biological physics and mechanics · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
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  11. Review
  12. Article
  13. Article
  14. Polymodal Sensory Transduction in Mouse Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2020
    Article
  15. 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

3 authors at 1 institution in 1 country.

Oleg YarishkinDepartment of Ophthalmology and Visual Sciences, University of Utah, Salt Lake City, Utah, United States.
Tam T T PhuongDepartment of Ophthalmology and Visual Sciences, University of Utah, Salt Lake City, Utah, United States.
David KrižajDepartment of Ophthalmology and Visual Sciences, University of Utah, Salt Lake City, Utah, United States.
University of Utah · US

Funding

University of Utah, Core Vision Research GrantP30EY014800 · NEI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Bryan William Jones · 2005 to 2026
$14.6M
Replacement of the Flexcell Tension systemR01EY027920 · NEI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI DAVID KRIZAJ · 2017 to 2026
$3.5M
The role of mechanosensation in the vertebrate retinaR01EY022076 · NEI · UNIVERSITY OF UTAH · PI KRIZAJ, DAVID · 2013 to 2017
$1.9M
NEI NIH HHS P30 EY014800NEI NIH HHS R01 EY022076NEI NIH HHS R01 EY027920
6 · The paper itself

Abstract

Purpose: The concentration of protons in the aqueous humor (AH) of the vertebrate eye is maintained close to blood pH; however, pathologic conditions and surgery may shift it by orders of magnitude. We investigated whether and how changes in extra- and intracellular pH affect the physiology and function of trabecular meshwork (TM) cells that regulate AH outflow. Methods: Electrophysiology, in conjunction with pharmacology, gene knockdown, and optical recording, was used to track the pH dependence of transmembrane currents and mechanotransduction in primary and immortalized human TM cells. Results: Extracellular acidification depolarized the resting membrane potential by inhibiting an outward K+-mediated current, whereas alkalinization hyperpolarized the cells and augmented the outward conductance. Intracellular acidification with sodium bicarbonate hyperpolarized TM cells, whereas removal of intracellular protons with ammonium chloride depolarized the membrane potential. The effects of extra- and intracellular acid and alkaline loading were abolished by quinine, a pan-selective inhibitor of two-pore domain potassium (K2P) channels, and suppressed by shRNA-mediated downregulation of the mechanosensitive K2P channel TREK-1. Extracellular acidosis suppressed, whereas alkalosis facilitated, the amplitude of the pressure-evoked TREK-1-mediated outward current. Conclusions: These results demonstrate that TM mechanotransduction mediated by TREK-1 channels is profoundly sensitive to extra- and intracellular pH shifts. Intracellular acidification might modulate aqueous outflow and IOP by stimulating TREK-1 channels.

Indexed as

Hydrogen-Ion ConcentrationPressureCells, CulturedHumansMechanotransduction, CellularMembrane PotentialsPatch-Clamp TechniquesPotassium Channels, Tandem Pore DomainTrabecular Meshworkpotassium channel protein TREK-1Potassium Channels, Tandem Pore Domain

Identifiers

PMID31117121
PMCPMC6532698
OpenAlexW2945384233

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.