Evidence map›Paper›PMID 21976958›Full record

ArticleMolecular vision2011

SOD2 contributes to anti-oxidative capacity in rabbit corneal endothelial cells.

Cailing Liu, Diego Ogando, Joseph A Bonanno

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Diabetes, metabolic syndrome and obesity : targets and therapy · 2018
    Article
  8. Astragalus polysaccharides improve cardiomyopathy in STZ-induced diabetic mice and heterozygous (SOD2+/-) knockout mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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 1 institution in 1 country.

Cailing LiuSchool of Optometry, Indiana University, Bloomington, IN, USA.
Diego Ogando
Joseph A Bonanno
Indiana University Bloomington · US

Funding

REGULATION OF PHI AND FLUID FLUX IN CORNEAL ENDOTHELIUMR01EY008834 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI BONANNO, JOSEPH AURELIO · 1991 to 2020
$7.8M
Core Support for Vision Research at Indiana UniversityP30EY019008 · NEI · TRUSTEES OF INDIANA UNIVERSITY · PI BURNS, STEPHEN A · 2009 to 2013
$2.1M
NEI NIH HHS P30 EY019008NEI NIH HHS P30EY019008NEI NIH HHS R01 EY008834NEI NIH HHS R01EY008834
6 · The paper itself

Abstract

purposeCorneal endothelial cells are rich in mitochondria, a potential source of reactive oxygen species (ROS). ROS have been implicated in endothelial cell loss during aging or in endothelial dystrophies. In this study we examined the anti-oxidative role of mitochondrial superoxide dismutase (SOD2) in corneal endothelial cells.

methodsSOD2 expression was examined by RT-PCR and western blot analysis in fresh rabbit corneal endothelium (RCE) and cell cultures. SOD2 activity, total reactive oxygen species (ROS), mitochondrial ROS, mitochondrial membrane potential (MMP), and apoptotic levels were examined in untreated, SOD2 siRNA and viral vector shRNA treated RCE cells. Scrambled siRNA and shRNA sequence targeting non-mammalian genes were used as controls.

resultsSOD2 is expressed in both fresh and cultured rabbit corneal endothelium. SOD2 expression was reduced by ~80%-90% in cultured RCE using either siRNA or shRNA approaches. SOD2 activity was decreased by ~70%-80% for both approaches. Total cell ROS was significantly increased in shSOD2 lentivirus treated cells (9%±6%) relative to control transduction (0.4%±0.1%). MitoSOX™ staining for mitochondrial ROS in siSOD2 treated RCE cells was dramatically increased. Two minutes of UV irradiation increased total ROS levels by 15%, whereas in shSOD2 treated cells UV induced ROS was increased 29%±5% (p<0.05). MMP was reduced in shSOD2 viral treated cells by 66%±3%, significantly greater than in control transduced cells (15%±8%, p<0.05). Apoptosis increased by 1.5 fold in shSOD2 virus treated samples compared with scrambled virus and untreated cells.

conclusionsSOD2 is expressed in both fresh and cultured rabbit corneal endothelium. siRNA and shRNA approaches are able to efficiently knockdown SOD2 expression and reduce enzyme activity in RCE cells. Decreased SOD2 activity causes elevated ROS production, mitochondrial membrane potential loss and early cell apoptosis. These results indicate that SOD2 is a significant anti-oxidative enzyme in RCE cells.

Indexed as

AnimalsAntioxidantsApoptosisBlotting, WesternCells, CulturedCorneaEndothelial CellsEndothelium, CornealGene ExpressionGene SilencingMembrane Potential, MitochondrialMitochondriaOxidative StressRabbitsReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionAntioxidantsReactive Oxygen SpeciesRNA, Small InterferingSuperoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID21976958
PMCPMC3185022
OpenAlexW2121393320

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.