Evidence map›Paper›PMID 28276476›Full record

ArticleScientific reports2017

miR-193a-3p interaction with HMGB1 downregulates human endothelial cell proliferation and migration.

Cheen P Khoo, Maria G Roubelakis, Jack B Schrader, Grigorios Tsaknakis, Rebecca Konietzny, Benedikt Kessler, Adrian L Harris, Suzanne M Watt

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The TBX1/miR-193a-3p/TGF-Oxidative medicine and cellular longevity · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors.

Cheen P KhooStem Cell Research, Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Oxford, OX3 9BQ, UK.
Maria G RoubelakisStem Cell Research, Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Oxford, OX3 9BQ, UK.
Jack B SchraderStem Cell Research, Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Oxford, OX3 9BQ, UK.
Grigorios TsaknakisStem Cell Research, Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Oxford, OX3 9BQ, UK.
Rebecca KonietznyTarget Discovery Institute, NDM Research Building, Nuffield Department of Medicine, University of Oxford, OX3 7FZ, UK.
Benedikt KesslerTarget Discovery Institute, NDM Research Building, Nuffield Department of Medicine, University of Oxford, OX3 7FZ, UK.
Adrian L HarrisThe Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.
Suzanne M WattStem Cell Research, Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Oxford, OX3 9BQ, UK.

Funding

Biotechnology and Biological Sciences Research CouncilCancer Research UK 11359Cancer Research UK 16466Cancer Research UK 18974Department of Health RP-PG-0310-1003Medical Research Council G0300648
6 · The paper itself

Abstract

Circulating endothelial colony forming cells (ECFCs) contribute to vascular repair where they are a target for therapy. Since ECFC proliferative potential is increased in cord versus peripheral blood and to define regulatory factors controlling this proliferation, we compared the miRNA profiles of cord blood and peripheral blood ECFC-derived cells. Of the top 25 differentially regulated miRNAs selected, 22 were more highly expressed in peripheral blood ECFC-derived cells. After validating candidate miRNAs by q-RT-PCR, we selected miR-193a-3p for further investigation. The miR-193a-3p mimic reduced cord blood ECFC-derived cell proliferation, migration and vascular tubule formation, while the miR-193a-3p inhibitor significantly enhanced these parameters in peripheral blood ECFC-derived cells. Using in silico miRNA target database analyses combined with proteome arrays and luciferase reporter assays of miR-193a-3p mimic treated cord blood ECFC-derived cells, we identified 2 novel miR-193a-3p targets, the high mobility group box-1 (HMGB1) and the hypoxia upregulated-1 (HYOU1) gene products. HMGB1 silencing in cord blood ECFC-derived cells confirmed its role in regulating vascular function. Thus, we show, for the first time, that miR-193a-3p negatively regulates human ECFC vasculo/angiogenesis and propose that antagonising miR-193a-3p in less proliferative and less angiogenic ECFC-derived cells will enhance their vasculo/angiogenic function.

Indexed as

Cell MovementCell ProliferationDown-RegulationEndothelial CellsEndothelial Progenitor CellsHMGB1 ProteinHumansMicroRNAsHMGB1 ProteinHMGB1 protein, humanMicroRNAsMIRN193 microRNA, human

Identifiers

PMID28276476
PMCPMC5343468

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.