Evidence map›Paper›PMID 31734278›Full record

ArticleExperimental eye research2020

Elevated ocular pressure reduces voltage-gated sodium channel NaV1.2 protein expression in retinal ganglion cell axons.

Michael L Risner, Nolan R McGrady, Silvia Pasini, Wendi S Lambert, David J Calkins

Open access · hybridAbstract read
In one paragraph

Article in Experimental eye research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  10. Adaptive responses to neurodegenerative stress in glaucoma.Progress in retinal and eye research · 2021
    Review
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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

5 authors at 1 institution in 1 country.

Michael L RisnerDepartment of Ophthalmology and Visual Sciences, Vanderbilt University Medical Center, 11435 Medical Research Building IV, 2215B Garland Ave, Nashville, TN, 37232-0654, USA.
Nolan R McGradyDepartment of Ophthalmology and Visual Sciences, Vanderbilt University Medical Center, 11435 Medical Research Building IV, 2215B Garland Ave, Nashville, TN, 37232-0654, USA.
Silvia PasiniDepartment of Ophthalmology and Visual Sciences, Vanderbilt University Medical Center, 11435 Medical Research Building IV, 2215B Garland Ave, Nashville, TN, 37232-0654, USA.
Wendi S LambertDepartment of Ophthalmology and Visual Sciences, Vanderbilt University Medical Center, 11435 Medical Research Building IV, 2215B Garland Ave, Nashville, TN, 37232-0654, USA.
David J CalkinsDepartment of Ophthalmology and Visual Sciences, Vanderbilt University Medical Center, 11435 Medical Research Building IV, 2215B Garland Ave, Nashville, TN, 37232-0654, USA. Electronic address: david.j.calkins@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
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
Mechanisms of Synaptic Remodeling and Neuronal Self-Repair in Aging and GlaucomaR01EY024997 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 2015 to 2026
$3.8M
NCI NIH HHS P30 CA068485NEI NIH HHS P30 EY008126NEI NIH HHS R01 EY017427NEI NIH HHS R01 EY024997NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Glaucoma is an age-related neurodegenerative disease that is commonly associated with sensitivity to intraocular pressure. The disease selectively targets retinal ganglion cells (RGCs) and constituent axons. RGC axons are rich in voltage-gated sodium channels, which are essential for action potential initiation and regeneration. Here, we identified voltage-dependent sodium channel, NaV1.2, in the retina, examined how this channel contributes to RGC light responses, and monitored NaV1.2 mRNA and protein expression in the retina during progression of modeled glaucoma. We found NaV1.2 is predominately localized in ganglion cell intraretinal axons with dispersed expression in the outer and inner plexiform layers. We showed Phrixotoxin-3, a potent NaV1.2 channel blocker, significantly decreased RGC electrical activity in a dose-dependent manner with an I

Indexed as

AnimalsAxonsGene Expression RegulationIntraocular PressureMaleMice, Inbred C57BLNAV1.2 Voltage-Gated Sodium ChannelOcular HypertensionRetinal Ganglion CellsRNA, MessengerTonometry, OcularNAV1.2 Voltage-Gated Sodium ChannelRNA, MessengerGlaucomaMicrobead occlusionNaV1.2Retinal ganglion cells

Identifiers

PMID31734278
PMCPMC6957720
OpenAlexW2986874830

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.