Evidence map›Paper›PMID 21282567›Full record

ArticleInvestigative ophthalmology & visual science2011

Opioid receptor activation: suppression of ischemia/reperfusion-induced production of TNF-α in the retina.

Shahid Husain, Gregory I Liou, Craig E Crosson

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  12. Changes in Class I and IIb HDACs by δ-Opioid in Chronic Rat Glaucoma Model.Investigative ophthalmology & visual science · 2020
    Article
  13. Article
  14. Article
  15. Neuroprotective Peptides in Retinal Disease.Journal of clinical medicine · 2019
    Review
  16. PI3K/Akt Pathway: A Role in δ-Opioid Receptor-Mediated RGC Neuroprotection.Investigative ophthalmology & visual science · 2017
    Article
  17. Article
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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

3 authors at 2 institutions in 1 country.

Shahid HusainHewitt Laboratory, Ola B. Williams Glaucoma Center, Department of Ophthalmology, Storm Eye Institute, Medical University of South Carolina, 167 Ashley Avenue, Charleston, SC 29425, USA. husain@musc.edu
Gregory I Liou
Craig E Crosson
Medical University of South Carolina · USAugusta University · US

Funding

MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
Protein Acetylation in Glaucomatous Optic NeuropathyR01EY021368 · NEI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CROSSON, CRAIG E. · 2011 to 2014
$1.4M
Opioidergic System: Its Role(s) in GlaucomaR01EY019081 · NEI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HUSAIN, SHAHID · 2010 to 2013
$1.4M
NCRR NIH HHS C06 RR015455NEI NIH HHS EY019081NEI NIH HHS EY021368NEI NIH HHS R01 EY019081NEI NIH HHS R01 EY021368
6 · The paper itself

Abstract

purposeThe detrimental role of TNF-α in ischemia-induced tissue damage is known. The authors study examined whether opioid receptor activation alters TNF-α levels in the postischemic retina.

methodsRetinal ischemia was induced by raising the intraocular pressure above systolic blood pressure (155-160 mm Hg) for 45 minutes. Rats were pretreated with the opioid receptor agonist morphine (1 mg/kg; intraperitoneally) before injury. Selected animals were pretreated with the opioid antagonist naloxone (3 mg/kg; intraperitoneally). Human optic nerve head (ONH) astrocytes and rat microglial cells were treated with morphine (0.1-1 μM) for 24 hours and then treated with 10 μg/mL or 30 ng/mL lipopolysaccharide (LPS), respectively. TNF-α was measured by ELISA. Opioid receptor subtypes in astrocytes and microglia were determined by Western blot analysis.

resultsThere was a time-dependent increase in TNF-α production; the maximum production occurred at 4 hours after ischemia and localized to the inner retinal regions. Ischemia-induced TNF-α production was significantly inhibited by morphine. In astrocytes and microglia, LPS triggered a robust increase in the release of TNF-α, which was significantly inhibited (P < 0.05) by morphine. Naloxone reversed the morphine-induced suppression of TNF-α production in vivo and in vitro. Both ONH astrocytes and microglial cells expressed δ-, κ-, and μ-opioid receptor subtypes.

conclusionsThese data provide evidence that the production of TNF-α after ischemia/reperfusion injury is an early event and that opioid receptor activation reduces the production of TNF-α. Immunohistochemistry data and in vitro studies provide evidence that ONH astrocytes and microglial cells are the primary sources for the TNF-α production under ischemic/inflammatory conditions. Activation of one or more opioid receptors can reduce ischemic/reperfusion injury by the suppression of TNF-α production.

Indexed as

AnimalsAstrocytesBlotting, WesternCells, CulturedEnzyme-Linked Immunosorbent AssayFemaleFluorescent Antibody Technique, IndirectLipopolysaccharidesMaleMicrogliaMorphineNaloxoneNarcotic AntagonistsOptic DiskRatsRats, Inbred BNLipopolysaccharidesMorphineNaloxoneNarcotic AntagonistsReceptors, OpioidTumor Necrosis Factor-alpha

Identifiers

PMID21282567
PMCPMC3088550
OpenAlexW2044408149

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.