Evidence map›Paper›PMID 21917933›Full record

ArticleInvestigative ophthalmology & visual science2011

Quantitative proteomics: TGFβ₂ signaling in trabecular meshwork cells.

Kathryn E Bollinger, John S Crabb, Xianglin Yuan, Tasneem Putliwala, Abbot F Clark, John W Crabb

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 69 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Kathryn E BollingerCole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
John S Crabb
Xianglin Yuan
Tasneem Putliwala
Abbot F Clark
John W Crabb
Cleveland Clinic · USThe California Eye Institute · USUniversity of North Texas · USUniversity of North Texas Health Science Center · US

Funding

Proteomic Studies of Age Related Macular DegenerationR01EY014239 · NEI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI CRABB, JOHN W · 2002 to 2005
$1.5M
Vision Research Infrastructure Development GrantR24EY015638 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI HOLLYFIELD, JOE GILBERT · 2004 to 2008
$1.1M
Proteomic Biomarkers for Primary Open Angle GlaucomaR21EY018147 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI CRABB, JOHN W · 2008 to 2009
$432k
NEI NIH HHS EY018147NEI NIH HHS EY14239NEI NIH HHS R01 EY014239NEI NIH HHS R21 EY018147NEI NIH HHS R24 EY015638
6 · The paper itself

Abstract

purposeTransforming growth factor beta 2 (TGFβ₂) is often elevated in the aqueous humor (AH) and trabecular meshwork (TM) of patients with primary open-angle glaucoma (POAG) and appears to contribute to POAG pathogenesis. To better understand TGFβ₂ signaling in the eye, TGFβ₂-induced proteomic changes were identified in cells cultured from the TM, a tissue involved in intraocular pressure (IOP) elevation in glaucoma.

methodsPrimary cultures of human TM cells from four donors were treated with or without TGFβ₂ (5 ng/mL) for 48 hours; then cellular protein was analyzed by liquid chromatography-mass spectrometry iTRAQ (isobaric tags for relative and absolute quantitation) technology.

resultsA total of 853 proteins were quantified. TGFβ₂ treatment significantly altered the abundance of 47 proteins, 40 of which have not previously been associated with TGFβ₂ signaling in the eye. More than half the 30 elevated proteins support growing evidence that TGFβ₂ induces extracellular matrix remodeling and abnormal cytoskeletal interactions in the TM. The levels of 17 proteins were reduced, including four cytoskeletal and six regulatory proteins. Both elevated and decreased regulatory proteins implicate TGFβ₂-altered processes involving transcription, translation, and the glutamate/glutamine cycle. Altered levels of eight mitochondrial proteins support TGFβ₂-induced mitochondrial dysfunction in the TM that in POAG could contribute to oxidative damage in the AH outflow pathway, TM senescence, and elevated IOP.

conclusionsThe results expand the repertoire of proteins known to participate in TGFβ₂ signaling, provide new molecular insight into POAG, and establish a quantitative proteomics database for the TM that includes candidate glaucoma biomarkers for future validation studies.

Indexed as

Eye ProteinsGlaucoma, Open-AngleHumansIntraocular PressureOcular HypertensionPeptidesPrimary Cell CultureProtein PrecursorsProteomicsSignal TransductionTrabecular MeshworkTransforming Growth Factor betaEye Proteinslatency-associated propeptide, TGF-betaPeptidesProtein PrecursorsTransforming Growth Factor beta

Identifiers

PMID21917933
PMCPMC3208113
OpenAlexW2089432090

What OpenQuestion holds

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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.