Evidence map›Paper›PMID 25802486›Full record

ArticleMolecular vision2015

MicroRNA-152 represses VEGF and TGFβ1 expressions through post-transcriptional inhibition of (Pro)renin receptor in human retinal endothelial cells.

Rashidul Haque, Elizabeth H Hur, Annie N Farrell, P Michael Iuvone, Jennifer C Howell

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. RAAS in diabetic retinopathy: mechanisms and therapies.Archives of endocrinology and metabolism · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. MicroRNA-15b Targets VEGF and Inhibits Angiogenesis in Proliferative Diabetic Retinopathy.The Journal of clinical endocrinology and metabolism · 2020
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

5 authors at 1 institution in 1 country.

Rashidul HaqueDepartment of Ophthalmology, Emory University School of Medicine, Atlanta, GA.
Elizabeth H HurDepartment of Ophthalmology, Emory University School of Medicine, Atlanta, GA.
Annie N FarrellDepartment of Ophthalmology, Emory University School of Medicine, Atlanta, GA.
P Michael IuvoneDepartment of Ophthalmology, Emory University School of Medicine, Atlanta, GA.
Jennifer C HowellDepartment of Ophthalmology, Emory University School of Medicine, Atlanta, GA.
Emory University · US

Funding

P30-Core Grant for Vision Research Core CP30EY006360 · NEI · EMORY UNIVERSITY · PI BOATRIGHT, JEFFREY H · 1986 to 2025
$15.3M
Neuromodulators and Circadian Clocks: Roles in Retinal Function and DysfunctionR01EY004864 · NEI · EMORY UNIVERSITY · PI IUVONE, P MICHAEL · 1985 to 2018
$7.0M
NEI NIH HHS P30 EY006360NEI NIH HHS P30EY006360NEI NIH HHS R01 EY004864NEI NIH HHS R01EY004864
6 · The paper itself

Abstract

purposeThe (pro)renin receptor (PRR), a component of the renin-angiotensin system (RAS), plays an important role in the physiologic and pathophysiological regulation of blood pressure and fluid/electrolyte homeostasis. The RAS including the PRR has been identified in retinal endothelial cells and other ocular tissues. In this study, the potential involvement of miRNAs in the posttranscriptional regulation of PRR was investigated in human retinal endothelial cells (hRECs) under high glucose (HG) conditions.

methodsmiRNA-152 (miR-152) was identified in silico as a potential regulator of PRR, and this was confirmed by quantitative real-time PCR (qRT-PCR) and PRR 3'-untranslated region (UTR) reporter assays. Using RNA interference, both AT1R and PRR were implicated in the HG-mediated induction of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR-2), and transforming growth factor β1 (TGFβ1).

resultsThe downregulation of miR-152 was observed in hRECs and rat retinal tissues under HG conditions. In parallel, PRR (target of miR-152), VEGF, VEGFR-2, and TGFβ1 at mRNA levels were elevated. However, the transfection of hRECs with miR-152 mimics in HG conditions resulted in the suppression of the PRR expression, as well as reduced VEGF, VEGFR-2, and TGFβ1 production. This was reversed by transfecting cells with the antisense (antagomir) of miR-152, suggesting the glucose-induced upregulation of VEGF, VEGFR-2, and TGFβ1 is mediated through PRR, and this regulation is likely achieved through the HG-mediated modulation of miRNAs.

conclusionsWe have demonstrated that miR-152 interacting with PRR regulates downstream VEGF, VRGFR-2, and TGFβ1 expressions in hRECs in HG conditions. These studies suggest miR-152 and PRR may play a role in the pathogenesis of diabetic retinopathy (DR).

Indexed as

3' Untranslated RegionsAnimalsCells, CulturedEndothelial CellsGlucoseHumansMaleMicroRNAsProrenin ReceptorRatsRats, Long-EvansReceptor, Angiotensin, Type 1Receptors, Cell SurfaceRenin-Angiotensin SystemRetinaRNA Interference3' Untranslated RegionsATP6AP2 protein, humanGlucoseKDR protein, humanMicroRNAsMIRN152 microRNA, humanProrenin ReceptorReceptor, Angiotensin, Type 1Receptors, Cell SurfaceTransforming Growth Factor beta1Vacuolar Proton-Translocating ATPasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2VEGFA protein, human

Identifiers

PMID25802486
PMCPMC4358229
OpenAlexW55560119

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.