Evidence map›Paper›PMID 21862656›Full record

ArticleInvestigative ophthalmology & visual science2011

The influence of alloxan-induced diabetes on Müller cell contraction-promoting activities in vitreous.

Jeffery L King, John O Mason, Samuel C Cartner, Clyde Guidry

Abstract 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

11 citing papers in PubMed.

  1. Review
  2. Pig Models in Retinal Research and Retinal Disease.Cold Spring Harbor perspectives in medicine · 2024
    Review
  3. Review
  4. Comparison of before versus after intravitreal bevacizumab injection, growth factor levels and fibrotic markers in vitreous samples from patients with proliferative diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Article
  5. Diabetic Retinopathy: From Animal Models to Cellular Signaling.International journal of molecular sciences · 2022
    Review
  6. Animal models of diabetic retinopathy.Annals of translational medicine · 2021
    Review
  7. Animal Models of Diabetic Retinopathy.Current diabetes reports · 2017
    Review
  8. Epo inhibits the fibrosis and migration of Müller glial cells induced by TGF-β and high glucose.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2016
    Article
  9. Review
  10. Article
  11. Article
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

4 authors.

Jeffery L KingDepartment of Ophthalmology University of Alabama School of Medicine, Birmingham, Alabama 35294, USA.
John O Mason
Samuel C Cartner
Clyde Guidry

Funding

The Insulin-Like Growth Factor System and Muller CellsR01EY013258 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GUIDRY, CLYDE R · 2001 to 2009
$1.9M
NEI NIH HHS EY13258NEI NIH HHS R01 EY013258
6 · The paper itself

Abstract

purposePrevious studies from this laboratory revealed that vitreous insulin-like growth factor biological activity increases in diabetes and that this change can precede the onset of proliferative diabetic retinopathy. The goal of this study was to characterize this phenomenon in an animal model of alloxan-induced diabetes.

methodsSwine made diabetic with intravenous alloxan were euthanized at times varying from 0 to 90 days. Vitreous samples from normal and diabetic swine were evaluated for changes in Müller cell contraction-promoting activity, the presence of insulin-like growth factor binding protein (IGFBP), and carbonic anhydrase-I and -II. Ocular tissues from these animals were also evaluated for changes in contraction-promoting growth factors and IGFBP message levels.

resultsAlloxan-induced diabetes is associated with significant increases in vitreous Müller cell contraction-promoting activity that are present in as few as 30 days and are sustained for at least 90 days. Biochemical studies revealed that the increases cannot be attributed to loss of growth factor-attenuating IGFBPs, changes in local expression of contraction-promoting growth factors, or vitreous hemorrhage.

conclusionsThe previously reported increases in Müller cell contraction-promoting activity detected in human diabetic vitreous are present in diabetic swine within 30 days of chemical induction. The increase does not appear to be attributable to loss of growth factor control, increases in local growth factor expression, or vitreous hemorrhage, suggesting that other mechanisms are involved. It is the authors' speculation that diabetes induces blood-vitreous barrier changes that allow a different subset of plasma proteins to enter vitreous fluids.

Indexed as

AlloxanAnimalsBlood GlucoseBlotting, WesternCarbonic Anhydrase ICarbonic Anhydrase IIDiabetes Mellitus, ExperimentalDiabetic RetinopathyFluorescent Antibody Technique, IndirectGlial Fibrillary Acidic ProteinHyperglycemiaInsulin-Like Growth Factor Binding ProteinsMaleNeurogliaReal-Time Polymerase Chain ReactionRetinaAlloxanBlood GlucoseCarbonic Anhydrase ICarbonic Anhydrase IIGlial Fibrillary Acidic ProteinInsulin-Like Growth Factor Binding Proteins

Identifiers

PMID21862656
PMCPMC3183978

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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.