Evidence map›Paper›PMID 28980000›Full record

ArticleInvestigative ophthalmology & visual science2017

Increased Indoleamine 2,3-Dioxygenase and Quinolinic Acid Expression in Microglia and Müller Cells of Diabetic Human and Rodent Retina.

Ping Hu, Nicholas H Hunt, Frank Arfuso, Lynn C Shaw, Mohammad Nasir Uddin, Meidong Zhu, Raj Devasahayam, Samuel J Adamson, Vicky L Benson, Tailoi Chan-Ling and 1 more

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 34% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Clinical Significance of Serum CCR2 and IDO1 in Diabetic Peripheral Neuropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Article
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021
    Review
  20. Review
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

11 authors at 5 institutions in 3 countries.

Ping HuDepartment of Anatomy, Bosch Institute, University of Sydney, New South Wales, Australia.
Nicholas H HuntDepartment of Pathology, Bosch Institute, University of Sydney, New South Wales, Australia.
Frank ArfusoDepartment of Anatomy, Bosch Institute, University of Sydney, New South Wales, Australia.
Lynn C ShawDepartment of Ophthalmology, the Eugene and Marilyn Glick Eye Institute, Indiana University, Indianapolis, Indiana, United States.
Mohammad Nasir UddinDepartment of Anatomy, Bosch Institute, University of Sydney, New South Wales, Australia.
Meidong ZhuLions New South Wales Eye Bank, New South Wales Organ and Tissue Donation Service, South Eastern Sydney Local Health District, New South Wales, Australia.
Raj DevasahayamLions New South Wales Eye Bank, New South Wales Organ and Tissue Donation Service, South Eastern Sydney Local Health District, New South Wales, Australia.
Samuel J AdamsonDepartment of Anatomy, Bosch Institute, University of Sydney, New South Wales, Australia.
Vicky L BensonDepartment of Physiology, Faculty of Health and Medical Sciences, University of Auckland, Auckland, New Zealand.
Tailoi Chan-LingDepartment of Anatomy, Bosch Institute, University of Sydney, New South Wales, Australia.
Maria B GrantDepartment of Ophthalmology, the Eugene and Marilyn Glick Eye Institute, Indiana University, Indianapolis, Indiana, United States.
Robert Bosch (Australia) · AUUniversity of Sydney · AUIndiana University – Purdue University Indianapolis · USSouth Eastern Sydney Local Health District · AUUniversity of Auckland · NZ

Funding

Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Carmella Evans-Molina · 2015 to 2026
$17.4M
NITRIC OXIDE IN THE PATHOGENESIS OF DIABETIC RETINOPATHYR01EY012601 · NEI · UNIVERSITY OF FLORIDA · PI Julia V Busik, Maria Bartolomeo Grant · 1998 to 2026
$9.6M
Targeting the IGF-1 System in Retinal AngiogenesisR01EY007739 · NEI · UNIVERSITY OF FLORIDA · PI ABCOUWER, STEVEN F, GRANT, MARIA BARTOLOMEO · 1995 to 2015
$5.4M
NO Dysregulation of the Peripheral Clock in Diabetic ComplicationsR01DK090730 · NIDDK · UNIVERSITY OF FLORIDA · PI GRANT, MARIA BARTOLOMEO · 2010 to 2013
$1.3M
NEI NIH HHS R01 EY007739NEI NIH HHS R01 EY012601NIDDK NIH HHS P30 DK097512NIDDK NIH HHS R01 DK090730
6 · The paper itself

Abstract

Purpose: We investigated the relationship between inflammation, neuronal loss, and expression of indoleamine 2, 3-dioxygenase (IDO) and quinolinic acid (QUIN) in the retina of subjects with type 1 diabetes (T1D) and type 2 diabetes (T2D) and in the retina of rats with T1D. Methods: Retinas from T1D (n = 7), T2D (n = 13), and 20 age-matched nondiabetic human donors and from T1D (n = 3) and control rats (n = 3) were examined using immunohistochemistry for IDO, QUIN, cluster of differentiation 39 (CD39), ionized calcium-binding adaptor molecule (Iba-1, for macrophages and microglia), Vimentin (VIM; for Müller cells), neuronal nuclei (NeuN; for neurons), and UEA1 lectin (for blood vessels). Results: Based on morphologic criteria, CD39+/ionized calcium binding adaptor molecule 1(Iba-1+) resident microglia and CD39-/Iba-1+ bone marrow-derived macrophages were present at higher density in T1D (13% increase) and T2D (26% increase) human retinas when compared with controls. The density and brightness of IDO+ microglia were increased in both T1D and T2D human retinas. The intensity of QUIN+ expression on CD39+ microglia and VIM+ Müller cells was greatly increased in both human T1D and T2D retinas. T1D retinas showed a 63% loss of NeuN+ neurons and T2D retinas lost approximately 43% when compared with nondiabetic human retinas. Few QUIN+ microglia-like cells were seen in nondiabetic retinas, but the numbers increased 18-fold in T1D and 7-fold in T2D in the central retina. In T1D rat retinas, the density of IDO+ microglia increased 2.8-fold and brightness increased 2.1-fold when compared with controls. Conclusions: Our findings suggest that IDO and QUIN expression in the retinas of diabetic rats and humans could contribute to the neuronal degeneration that is characteristic of diabetic retinopathy.

Indexed as

AgedAnimalsAntigens, CDAntigens, NuclearApyraseBiomarkersCalcium-Binding ProteinsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic RetinopathyDNA-Binding ProteinsEpendymoglial CellsFemaleFluorescent Antibody Technique, IndirectHumansAIF1 protein, humanAif1 protein, ratAntigens, CDAntigens, NuclearApyraseBiomarkersCalcium-Binding ProteinsCD39 antigenDNA-Binding ProteinsIndoleamine-Pyrrole 2,3,-DioxygenaseMicrofilament ProteinsNerve Tissue Proteinsneuronal nuclear antigen NeuN, humanQuinolinic AcidRbfox3 protein, ratVimentin

Identifiers

PMID28980000
PMCPMC5633007
OpenAlexW2740350297

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.