Evidence map›Paper›PMID 18952924›Full record

ArticleInvestigative ophthalmology & visual science2009

TRPV1: contribution to retinal ganglion cell apoptosis and increased intracellular Ca2+ with exposure to hydrostatic pressure.

Rebecca M Sappington, Tatiana Sidorova, Daniel J Long, David J Calkins

Open access · greenAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

121 citing papers in PubMed, 196 citations in OpenAlex.

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  10. Capsaicin: Emerging Pharmacological and Therapeutic Insights.Current issues in molecular biology · 2024
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  12. The Healthy and Diseased Retina Seen through Neuron-Glia Interactions.International journal of molecular sciences · 2024
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  15. Integrated virtual screening andFrontiers in pharmacology · 2024
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  18. Therapeutic Potential of Cannabinoids in Glaucoma.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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61 more citing papers are in PubMed but not listed here.

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.

Rebecca M SappingtonVanderbilt Eye Institute, Vanderbilt University Medical Center, Nashville, Tennessee 37232-0654, USA.
Tatiana Sidorova
Daniel J Long
David J Calkins
Vanderbilt University Medical Center · US

Funding

Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
Transient Receptor Potential Channels and Retinal Ganglion Cell Death in GlaucomaR01EY017427 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CALKINS, DAVID J. · 2008 to 2020
$4.2M
NEI NIH HHS 5P30EY008126-19NEI NIH HHS EY017427NEI NIH HHS P30 EY008126NEI NIH HHS R01 EY017427
6 · The paper itself

Abstract

purposeElevated hydrostatic pressure induces retinal ganglion cell (RGC) apoptosis in culture. The authors investigated whether the transient receptor potential vanilloid 1 (TRPV1) channel, which contributes to pressure sensing and Ca(2+)-dependent cell death in other systems, also contributes to pressure-induced RGC death and whether this contribution involves Ca(2+).

methodstrpv1 mRNA expression in RGCs was probed with the use of PCR and TRPV1 protein localization through immunocytochemistry. Subunit-specific antagonism (iodo-resiniferatoxin) and agonism (capsaicin) were used to probe how TRPV1 activation affects the survival of isolated RGCs at ambient and elevated hydrostatic pressure (+70 mm Hg). Finally, for RGCs under pressure, the authors tested whether EGTA chelation of Ca(2+) improves survival and whether, with the Ca(2+) dye Fluo-4 AM, TRPV1 contributes to increased intracellular Ca(2+).

resultsRGCs express trpv1 mRNA, with robust TRPV1 protein localization to the cell body and axon. For isolated RGCs under pressure, TRPV1 antagonism increased cell density and reduced apoptosis to ambient levels (P <or= 0.05), whereas for RGCs at ambient pressure, TRPV1 agonism reduced density and increased apoptosis to levels for elevated pressure (P <or= 0.01). Chelation of extracellular Ca(2+) reduced RGC apoptosis at elevated pressure by nearly twofold (P <or= 0.01). Exposure to elevated hydrostatic pressure induced a fourfold increase in RGC intracellular Ca(2+) that was reduced by half with TRPV1 antagonism. Finally, in the DBA/2 mouse model of glaucoma, levels of TRPV1 in RGCs increased with elevated IOP.

conclusionsRGC apoptosis induced by elevated hydrostatic pressure arises substantially through TRPV1, likely through the influx of extracellular Ca(2+).

Indexed as

ApoptosisHydrostatic PressureAnimalsAxonsBlotting, WesternCalciumDiterpenesIn Situ HybridizationIntraocular PressureMiceMice, Inbred C57BLMice, Inbred DBAMicroscopy, FluorescenceRatsRats, Sprague-DawleyRetinal Ganglion CellsCalciumDiterpenesiodoresiniferatoxinRNA, MessengerTRPV1 protein, mouseTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID18952924
PMCPMC3549616
OpenAlexW2028023737

What OpenQuestion holds

Textmetadata
LicenceTDM
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.