Evidence map›Paper›PMID 30981984›Full record

ArticleMolecular therapy. Nucleic acids2019

MicroRNA-145 Regulates Pathological Retinal Angiogenesis by Suppression of TMOD3.

Chi-Hsiu Liu, Zhongxiao Wang, Shuo Huang, Ye Sun, Jing Chen

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. 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
1.5field-weighted citation impact, top 21% 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, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Systemic Cytokines in Retinopathy of Prematurity.Journal of personalized medicine · 2023
    Review
  11. MicroRNAs in the Mouse Developing Retina.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

5 authors at 2 institutions in 1 country.

Chi-Hsiu LiuDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Zhongxiao WangDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Shuo HuangDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Ye SunDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Jing ChenDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. Electronic address: jing.chen@childrens.harvard.edu.
Harvard University · USBoston Children's Hospital · US

Funding

RORalpha mediates chronic subretinal inflammation associated with AMDR01EY024963 · NEI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, JING · 2015 to 2025
$4.2M
Wnt signaling-mediated control of blood-retinal barrierR01EY028100 · NEI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, JING · 2017 to 2021
$2.2M
NEI NIH HHS R01 EY024963NEI NIH HHS R01 EY028100
6 · The paper itself

Abstract

Pathological angiogenesis is a hallmark of various vascular diseases, including vascular eye disorders. Dysregulation of microRNAs (miRNAs), a group of small regulatory RNAs, has been implicated in the regulation of ocular neovascularization. This study investigated the specific role of microRNA-145 (miR-145) in regulating vascular endothelial cell (EC) function and pathological ocular angiogenesis in a mouse model of oxygen-induced retinopathy (OIR). Expression of miR-145 was significantly upregulated in OIR mouse retinas compared with room air controls. Treatment with synthetic miR-145 inhibitors drastically decreased levels of pathological neovascularization in OIR, without substantially affecting normal developmental angiogenesis. In cultured human retinal ECs, treatment with miR-145 mimics significantly increased the EC angiogenic function, including proliferation, migration, and tubular formation, whereas miR-145 inhibitors attenuated in vitro angiogenesis. Tropomodulin3 (TMOD3), an actin-capping protein, is a direct miR-145 target and is downregulated in OIR retinas. Treatment with miR-145 mimic led to TMOD3 inhibition, altered actin cytoskeletal architecture, and elongation of ECs. Moreover, inhibition of TMOD3 promoted EC angiogenic function and pathological neovascularization in OIR and abolished the vascular effects of miR-145 inhibitors in vitro and in vivo. Overall, our findings indicate that miR-145 is a novel regulator of TMOD3-dependent cytoskeletal architecture and pathological angiogenesis and a potential target for development of treatments for neovascular eye disorders.

Indexed as

angiogenesisendothelial cellmicroRNAmiR-145neovascularizationretinopathyTmod3

Identifiers

PMID30981984
PMCPMC6460252
OpenAlexW2923133198

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.