Evidence mapPaperPMID 24722243Full record

ArticleDiabetes2014

Parp inhibition prevents ten-eleven translocase enzyme activation and hyperglycemia-induced DNA demethylation.

Nyembezi Dhliwayo, Michael P Sarras, Ernest Luczkowski, Samantha M Mason, Robert V Intine

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  14. Combinatorial regulation of hepatic cytoplasmic signaling and nuclear transcriptional events by the OGT/REV-ERBα complex.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. Article
  16. Epigenetic Modification of MicroRNA-200b Contributes to Diabetic Vasculopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
  17. Review
  18. Article
  19. Review
  20. Dynamic DNA methylation of matrix metalloproteinase-9 in the development of diabetic retinopathy.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Nyembezi DhliwayoDr. William M. Scholl College of Podiatric Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, IL.
Michael P SarrasDepartment of Cell Biology and Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL.
Ernest LuczkowskiDr. William M. Scholl College of Podiatric Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, IL.
Samantha M MasonDr. William M. Scholl College of Podiatric Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, IL.
Robert V IntineDr. William M. Scholl College of Podiatric Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, IL Department of Cell Biology and Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL robert.intine@rosalindfranklin.edu.
Rosalind Franklin University of Medicine and Science · US

Funding

Epigenetic Mechanisms of Diabetic Metabolic Memory as Studies in Adult ZebrafishR21DK092721 · NIDDK · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI INTINE, ROBERT VICTOR · 2011 to 2012
$425k
NIDDK NIH HHS DK-092721NIDDK NIH HHS R21 DK092721
6 · The paper itself

Abstract

Studies from human cells, rats, and zebrafish have documented that hyperglycemia (HG) induces the demethylation of specific cytosines throughout the genome. We previously documented that a subset of these changes become permanent and may provide, in part, a mechanism for the persistence of complications referred to as the metabolic memory phenomenon. In this report, we present studies aimed at elucidating the molecular machinery that is responsible for the HG-induced DNA demethylation observed. To this end, RNA expression and enzymatic activity assays indicate that the ten-eleven translocation (Tet) family of enzymes are activated by HG. Furthermore, through the detection of intermediates generated via conversion of 5-methyl-cytosine back to the unmethylated form, the data were consistent with the use of the Tet-dependent iterative oxidation pathway. In addition, evidence is provided that the activity of the poly(ADP-ribose) polymerase (Parp) enzyme is required for activation of Tet activity because the use of a Parp inhibitor prevented demethylation of specific loci and the accumulation of Tet-induced intermediates. Remarkably, this inhibition was accompanied by a complete restoration of the tissue regeneration deficit that is also induced by HG. The ultimate goal of this work is to provide potential new avenues for therapeutic discovery.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsAnimal FinsAnimalsDiabetes Mellitus, ExperimentalDioxygenasesDisease Models, AnimalDNADNA MethylationEnzyme ActivationHyperglycemiaIsoquinolinesQuinolinesRegenerationZebrafishZebrafish Proteins1,5-dihydroxyisoquinolineDioxygenasesDNAIsoquinolinesPoly(ADP-ribose) Polymerase InhibitorsQuinolinesZebrafish Proteins

Identifiers

PMID24722243
PMCPMC4141369
OpenAlexW2100997565

What Socratic 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 Socratic graph.