Evidence map›Paper›PMID 23364452›Full record

ArticleDiabetes2013

The protective effects of CD39 overexpression in multiple low-dose streptozotocin-induced diabetes in mice.

Joanne S J Chia, Jennifer L McRae, Helen E Thomas, Stacey Fynch, Lorraine Elkerbout, Prue Hill, Lisa Murray-Segal, Simon C Robson, Jiang-Fan Chen, Anthony J F d'Apice and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Diabetes and hypertension: Pivotal involvement of purinergic signaling.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  3. Adenosine Signaling in Autoimmune Disorders.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. The influence of gut-derived CD39 regulatory T cells in CNS demyelinating disease.Translational research : the journal of laboratory and clinical medicine · 2017
    Review
  10. Article
  11. Unlocking the Potential of Purinergic Signaling in Transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016
    Review
  12. Role of the CD39/CD73 Purinergic Pathway in Modulating Arterial Thrombosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2016
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. CD39 and CD73 in immunity and inflammation.Trends in molecular medicine · 2013
    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

12 authors at 5 institutions in 2 countries.

Joanne S J ChiaImmunology Research Centre, St Vincent's Hospital, Melbourne, Victoria, Australia.
Jennifer L McRae
Helen E Thomas
Stacey Fynch
Lorraine Elkerbout
Prue Hill
Lisa Murray-Segal
Simon C Robson
Jiang-Fan Chen
Anthony J F d'Apice
Peter J Cowan
Karen M Dwyer
St Vincent's Hospital · AUSt Vincents Institute of Medical Research · AUUniversity of Melbourne · AUBeth Israel Deaconess Medical Center · USBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Islet allograft survival limits the long-term success of islet transplantation as a potential curative therapy for type 1 diabetes. A number of factors compromise islet survival, including recurrent diabetes. We investigated whether CD39, an ectonucleotidase that promotes the generation of extracellular adenosine, would mitigate diabetes in the T cell-mediated multiple low-dose streptozotocin (MLDS) model. Mice null for CD39 (CD39KO), wild-type mice (WT), and mice overexpressing CD39 (CD39TG) were subjected to MLDS. Adoptive transfer experiments were performed to delineate the efficacy of tissue-restricted overexpression of CD39. The role of adenosine signaling was examined using mutant mice and pharmacological inhibition. The susceptibility to MLDS-induced diabetes was influenced by the level of expression of CD39. CD39KO mice developed diabetes more rapidly and with higher frequency than WT mice. In contrast, CD39TG mice were protected. CD39 overexpression conferred protection through the activation of adenosine 2A receptor and adenosine 2B receptor. Adoptive transfer experiments indicated that tissue-restricted overexpression of CD39 conferred robust protection, suggesting that this may be a useful strategy to protect islet grafts from T cell-mediated injury.

Indexed as

AnimalsAntigens, CDApyraseDiabetes Mellitus, ExperimentalFlow CytometryImmunohistochemistryMaleMiceMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionReceptors, Purinergic P1Antigens, CDApyraseCD39 antigenReceptors, Purinergic P1

Identifiers

PMID23364452
PMCPMC3661652
OpenAlexW2167992945

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.