Evidence map›Paper›PMID 27239699›Full record

ArticleBiochimica et biophysica acta2016

Treatment with polyamine oxidase inhibitor reduces microglial activation and limits vascular injury in ischemic retinopathy.

C Patel, Z Xu, E Shosha, J Xing, R Lucas, R W Caldwell, R B Caldwell, S P Narayanan

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  2. Targeting adenosine APurinergic signalling · 2025
    Review
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  17. Article
  18. Polyamine Catabolism in Acute Kidney Injury.International journal of molecular sciences · 2019
    Review
  19. 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

8 authors at 1 institution in 1 country.

C PatelVision Discovery Institute, Augusta University, Augusta, GA 30912, USA; Vascular Biology Center, Augusta University, Augusta, GA 30912, USA; Department of Occupational Therapy, College of Allied Health Sciences, Augusta University, Augusta, GA 30912, USA. Electronic address: cpatel1@augusta.edu.
Z XuVision Discovery Institute, Augusta University, Augusta, GA 30912, USA; Vascular Biology Center, Augusta University, Augusta, GA 30912, USA. Electronic address: zhxu@augusta.edu.
E ShoshaVision Discovery Institute, Augusta University, Augusta, GA 30912, USA; Vascular Biology Center, Augusta University, Augusta, GA 30912, USA; Charlie Norwood VA Medical Center, Augusta, GA, USA. Electronic address: eshosha@augusta.edu.
J XingVision Discovery Institute, Augusta University, Augusta, GA 30912, USA; Vascular Biology Center, Augusta University, Augusta, GA 30912, USA. Electronic address: jxing8733@163.com.
R LucasVascular Biology Center, Augusta University, Augusta, GA 30912, USA; Department of Pharmacology & Toxicology, Augusta University, Augusta, GA 30912, USA. Electronic address: rlucas@augusta.edu.
R W CaldwellDepartment of Pharmacology & Toxicology, Augusta University, Augusta, GA 30912, USA. Electronic address: wcaldwel@augusta.edu.
R B CaldwellVision Discovery Institute, Augusta University, Augusta, GA 30912, USA; Vascular Biology Center, Augusta University, Augusta, GA 30912, USA; Department of Cellular Biology and Anatomy, Augusta University, Augusta, GA 30912, USA; Charlie Norwood VA Medical Center, Augusta, GA, USA. Electronic address: rcaldwel@augusta.edu.
S P NarayananVision Discovery Institute, Augusta University, Augusta, GA 30912, USA; Vascular Biology Center, Augusta University, Augusta, GA 30912, USA; Department of Occupational Therapy, College of Allied Health Sciences, Augusta University, Augusta, GA 30912, USA. Electronic address: pnarayanan@augusta.edu.
Augusta University · US

Funding

Cellular Mechanisms of Retinopathy: Role of ArginaseR01EY011766 · NEI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI CALDWELL, ROBERT WILLIAM, CALDWELL, RUTH B · 1998 to 2021
$6.7M
Mechanisms of Diabetic Retinopathy: Oxidative Stress and InflammationI01BX001233 · VA · CHARLIE NORWOOD VA MEDICAL CENTER · PI CALDWELL, RUTH B · 2012 to 2015
–
Mechanisms of Traumatic Retinal Injury: Targeting the Arginase PathwayI01BX003221 · VA · CHARLIE NORWOOD VA MEDICAL CENTER · PI CALDWELL, RUTH B · 2016 to 2019
–
American Heart Association-American Stroke Association 11SDG7440088BLRD VA I01 BX001233BLRD VA I01 BX003221NEI NIH HHS R01 EY011766
6 · The paper itself

Abstract

Retinal vascular injury is a major cause of vision impairment in ischemic retinopathies. Insults such as hyperoxia, oxidative stress and inflammation contribute to this pathology. Previously, we showed that hyperoxia-induced retinal neurodegeneration is associated with increased polyamine oxidation. Here, we are studying the involvement of polyamine oxidases in hyperoxia-induced injury and death of retinal vascular endothelial cells. New-born C57BL6/J mice were exposed to hyperoxia (70% O2) from postnatal day (P) 7 to 12 and were treated with the polyamine oxidase inhibitor MDL 72527 or vehicle starting at P6. Mice were sacrificed after different durations of hyperoxia and their retinas were analyzed to determine the effects on vascular injury, microglial cell activation, and inflammatory cytokine profiling. The results of this analysis showed that MDL 72527 treatment significantly reduced hyperoxia-induced retinal vascular injury and enhanced vascular sprouting as compared with the vehicle controls. These protective effects were correlated with significant decreases in microglial activation as well as levels of inflammatory cytokines and chemokines. In order to model the effects of polyamine oxidation in causing microglial activation in vitro, studies were performed using rat brain microvascular endothelial cells treated with conditioned-medium from rat retinal microglia stimulated with hydrogen peroxide. Conditioned-medium from activated microglial cultures induced cell stress signals and cell death in microvascular endothelial cells. These studies demonstrate the involvement of polyamine oxidases in hyperoxia-induced retinal vascular injury and retinal inflammation in ischemic retinopathy, through mechanisms involving cross-talk between endothelial cells and resident retinal microglia.

Indexed as

AnimalsCell DeathCell DifferentiationCells, CulturedCulture Media, ConditionedDisease Models, AnimalEnzyme InhibitorsFemaleInflammationIschemiaMaleMiceMice, Inbred C57BLMicrogliaOxidoreductases Acting on CH-NH Group DonorsPolyamine OxidaseCulture Media, ConditionedEnzyme InhibitorsMDL 72527Oxidoreductases Acting on CH-NH Group DonorsPolyamine OxidasePutrescine

Identifiers

PMID27239699
PMCPMC5091072
OpenAlexW2394648753

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.