Evidence map›Paper›PMID 19491369›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2009

Gene and protein expression pilot profiling and biomarkers in an experimental mouse model of hypertensive glaucoma.

Molly M Walsh, Haiqing Yi, Julie Friedman, Kyoung-In Cho, Nomingerel Tserentsoodol, Stuart McKinnon, Kelly Searle, Andrew Yeh, Paulo A Ferreira

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2009. 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
1.9field-weighted citation impact, top 14% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Discovery and clinical translation of novel glaucoma biomarkers.Progress in retinal and eye research · 2021
    Review
  4. Autophagy in the Aging and Experimental Ocular Hypertensive Mouse Model.Investigative ophthalmology & visual science · 2020
    Article
  5. Article
  6. Molecular Biomarkers for Glaucoma.Current ophthalmology reports · 2019
    Article
  7. Review
  8. Review
  9. Review
  10. Differential gene expression in glaucoma.Cold Spring Harbor perspectives in medicine · 2014
    Review
  11. Review
  12. Review
  13. Article
  14. 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

9 authors at 2 institutions in 1 country.

Molly M WalshDuke University Medical Center, Erwin Rd, DUEC 3802, Durham, NC 27710, USA. molly.walsh@duke.edu
Haiqing Yi
Julie Friedman
Kyoung-In Cho
Nomingerel Tserentsoodol
Stuart McKinnon
Kelly Searle
Andrew Yeh
Paulo A Ferreira
Duke University Hospital · USDuke Medical Center · US

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
NEI Mentored Clincial Scientist Development Program Award (K12)K12EY016333 · NEI · DUKE UNIVERSITY · PI COUSINS, SCOTT W · 2004 to 2013
$5.4M
NEI NIH HHS 2P30-EY005722-21NEI NIH HHS K12 EY016333NEI NIH HHS K12EY 302-8113NEI NIH HHS P30 EY005722
6 · The paper itself

Abstract

Glaucoma is a group of genetically heterogeneous neurodegenerative disorders causing the degeneration of the ganglion neurons of the retina. Increased intraocular pressure (IOP) is a hallmark risk factor promoting the death of ganglion neurons of the retina in glaucoma. Yet, the molecular processes underlying the degeneration of these neurons by increased IOP are not understood. To gain insight into the early molecular events and discover biomarkers induced by IOP, we performed gene and protein expression profiling to compare retinas of eyes with and without high IOP in a rodent model of experimental glaucoma. This pilot study found that the IOP-mediated changes in the transcription levels of a restricted set of genes implicated in peroxisomal and mitochondrial function, modulation of neuron survival and inflammatory processes, were also accompanied by changes in the levels of proteins encoded by the same genes. With the exception of the inflammatory markers, serum amyloid-A1 (SAA1) and serum amyloid-A2 (SAA2), the IOP-induced changes in protein expression were restricted to ganglion neurons of the retina and they were detected also in the vitreous, thus suggesting an early IOP-mediated loss of ganglion cell integrity. Interestingly, SAA1 and SAA2 were induced in retinal microglia cells, whereas they were reduced in sera of IOP-responsive mice. Hence, this study defines novel IOP-induced molecular processes, biomarkers and sources thereof, and it further validates the extension of the analyses herein reported to other genes modulated by IOP.

Indexed as

Gene Expression ProfilingAnimalsDisease Models, AnimalGene Expression RegulationGlaucomaHydrogen PeroxideImmunohistochemistryIntraocular PressureMiceMicrogliaNeuronsOcular HypertensionRetinaHydrogen Peroxide

Identifiers

PMID19491369
PMCPMC3697862
OpenAlexW2103344196

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.