Evidence map›Paper›PMID 21850156›Full record

ArticleMolecular vision2011

Increased tumor necrosis factor-α, cleaved caspase 3 levels and insulin receptor substrate-1 phosphorylation in the β₁-adrenergic receptor knockout mouse.

Surekha Rani Panjala, Youde Jiang, Timothy S Kern, Steven A Thomas, Jena J Steinle

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  8. IGFBP-3 and TNF-α regulate retinal endothelial cell apoptosis.Investigative ophthalmology & visual science · 2013
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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.

Surekha Rani PanjalaDepartment of Ophthalmology, Hamilton Eye Institute, The University of Tennessee Health Science Center, Memphis, TN, USA.
Youde Jiang
Timothy S Kern
Steven A Thomas
Jena J Steinle
University of Tennessee Health Science Center · US

Funding

STUDY OF DIABETIC RETINOPATHYR01EY000300 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI KERN, TIMOTHY S · 1985 to 2013
$4.7M
CORE--MOLECULAR BIOLOGYP30EY013080 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI JOHNSON, DIANNA AMMONS · 2000 to 2010
$3.7M
Molecular mechanisms of memrory retrievalR01MH063352 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI THOMAS, STEVEN A · 2002 to 2011
$3.2M
Vision Research CoreP30EY021721 · NEI · UNIVERSITY OF FLORIDA · PI HAUSWIRTH, WILLIAM W · 2011 to 2015
$2.8M
Study of diabetic retinopathyR56EY000300 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI KERN, TIMOTHY S · 2009 to 2009
$353k
NEI NIH HHS 3P30 EY013080NEI NIH HHS EY00300NEI NIH HHS P30 EY013080NEI NIH HHS P30 EY021721NEI NIH HHS R01 EY000300NEI NIH HHS R56 EY000300NIMH NIH HHS 5R01MH063352NIMH NIH HHS R01 MH063352
6 · The paper itself

Abstract

purposeTo investigate the role of β1-adrenergic receptors on insulin like growth factor (IGF)-1 receptor signaling and apoptosis in the retina using β1-adrenergic receptor knockout (KO) mice.

methodsWestern blotting and enzyme-linked immunosorbent assay analyses were done on whole retinal lysates from β1-adrenergic receptor KO mice and wild-type littermates. In addition, vascular analyses of degenerate capillaries and pericyte ghosts were done on the retina of the β1-adrenergic receptor KO mice versus littermates.

resultsLack of β1-adrenergic receptors produced a significant increase in both degenerate capillaries and pericyte ghosts. This was accompanied by an increase in cleaved caspase 3 and tumor necrosis factor α levels. IGF-1 receptor phosphorylation was not changed; however, protein kinase B (Akt) phosphorylation was significantly decreased. The decrease in Akt phosphorylation is likely caused by increased insulin receptor substrate-1 serine 307 (IRS-1(Ser307)) phosphorylation, which is inhibitory to IGF-1 receptor signaling.

conclusionsThese studies further support the idea that maintenance of β-adrenergic receptor signaling is beneficial for retinal homeostasis. Loss of β1-adrenergic receptor signaling alters tumor necrosis factor α and apoptosis levels in the retina, as well as Akt and IGF-1 receptor phosphorylation. Since many of these same changes are observed in the diabetic retina, these data support that novel β-adrenergic receptor agents may provide additional avenues for therapeutics.

Indexed as

Signal TransductionAnimalsApoptosisBlotting, WesternCapillariesCaspase 3Cell ExtractsDiabetes ComplicationsDiabetes MellitusDiabetic RetinopathyEnzyme-Linked Immunosorbent AssayHumansInsulin Receptor Substrate ProteinsMiceMice, KnockoutPericytesCaspase 3Cell ExtractsInsulin Receptor Substrate ProteinsProto-Oncogene Proteins c-aktReceptors, Adrenergic, beta-1SerineTumor Necrosis Factor-alpha

Identifiers

PMID21850156
PMCPMC3137556
OpenAlexW2148149909

What OpenQuestion holds

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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.