Evidence map›Paper›PMID 22110065›Full record

ArticleInvestigative ophthalmology & visual science2011

Role of β-adrenergic receptor regulation of TNF-α and insulin signaling in retinal Muller cells.

Robert J Walker, Nancy M Anderson, Youde Jiang, Suleiman Bahouth, Jena J Steinle

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. BetaScandinavian journal of medicine & science in sports · 2022
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  9. TLR4 regulates insulin-resistant proteins to increase apoptosis in the mouse retina.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
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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.

Robert J WalkerDepartment of Ophthalmology, Hamilton Eye Institute, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
Nancy M Anderson
Youde Jiang
Suleiman Bahouth
Jena J Steinle
Cincinnati Eye Institute · US

Funding

CORE--MOLECULAR BIOLOGYP30EY013080 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI JOHNSON, DIANNA AMMONS · 2000 to 2010
$3.7M
Vision Research CoreP30EY021721 · NEI · UNIVERSITY OF FLORIDA · PI HAUSWIRTH, WILLIAM W · 2011 to 2015
$2.8M
Beta-Adrenergic Receptor Modulation of Insulin SignalingF31EY019240 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WALKER, ROBERT · 2008 to 2012
$101k
NEI NIH HHS 3P30 EY013080NEI NIH HHS F31 EY019240NEI NIH HHS F31EY019240-02NEI NIH HHS P30 EY013080NEI NIH HHS P30 EY021721
6 · The paper itself

Abstract

purposeThe goal of this study was to determine the relationship of TNF-α and the downregulation of insulin receptor signaling in retinal Müller cells cultured under hyperglycemic conditions and the role of β-adrenergic receptors in regulating these responses.

methodsRetinal Müller cells were cultured in normal (5 mM) or high (25 mM) glucose until 80% confluent and then were reduced to 2% serum for 18 to 24 hours. The cells were then treated with 10 μM salmeterol followed by Western blot analysis or ELISA. For TNF-α inhibitory studies, the cells were treated with 5 ng/mL of TNF-α for 30 minutes or by a 30-minute pretreatment with TNF-α followed by salmeterol for 6 hours. In the TNF-α short hairpin (sh)RNA experiments, the cells were cultured until 90% confluent, followed by transfection with TNF-α shRNA for 18 hours.

resultsTNF-α-only treatments of Müller cells resulted in significant decreases of tyrosine phosphorylation of the insulin receptor and Akt in high-glucose conditions. Salmeterol (10 μM), a β-2-adrenergic receptor agonist, significantly increased phosphorylation of both insulin receptor and Akt. TNF-α shRNA significantly decreased phosphorylation of IRS-1(Ser307), which was further decreased after salmeterol+TNF-α shRNA. Both TNF-α shRNA and salmeterol significantly reduced death of the retinal Müller cells.

conclusionsThese studies demonstrate that β-adrenergic receptor agonists in vitro can restore the loss of insulin receptor activity noted in diabetes. By decreasing the levels of TNF-α and decreasing the phosphorylation of IRS-1(Ser307) while increasing tyrosine phosphorylation of insulin receptor, these results suggest a possible mechanism by which restoration of β-adrenergic receptor signaling may protect the retina against diabetes-induced damage.

Indexed as

Adrenergic beta-2 Receptor AgonistsAlbuterolAnimalsApoptosisBlotting, WesternCaspase 3Cells, CulturedDown-RegulationEnzyme-Linked Immunosorbent AssayHyperglycemiaInsulin Receptor Substrate ProteinsNeurogliaPhosphorylationProto-Oncogene Proteins c-aktRatsRetinaAdrenergic beta-2 Receptor AgonistsAlbuterolCaspase 3Insulin Receptor Substrate ProteinsIRS1 protein, humanProto-Oncogene Proteins c-aktSalmeterol XinafoateTumor Necrosis Factor-alpha

Identifiers

PMID22110065
PMCPMC3341119
OpenAlexW2159009152

What OpenQuestion holds

Textmetadata
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.