Evidence map›Paper›PMID 26539029›Full record

ArticleMolecular vision2015

Down-regulation of microRNA-155 attenuates retinal neovascularization via the PI3K/Akt pathway.

Zhi Zhuang, Xiao-qin, He Hu, Shi-yuan Tian, Zhan-jun Lu, Tian-zi Zhang, Yu-ling Bai

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021
    Review
  20. MicroRNAs in Vascular Eye Diseases.International journal of molecular sciences · 2020
    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

7 authors at 1 institution in 1 country.

Zhi ZhuangMedical College, Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
Xiao-qinDepartment of Ophthalmology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
He HuMedical College, Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
Shi-yuan TianDepartment of Ophthalmology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
Zhan-jun LuDepartment of Ophthalmology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
Tian-zi ZhangDepartment of Ophthalmology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
Yu-ling BaiDepartment of Ophthalmology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao Inner Mongolia, China.
Inner Mongolia University for Nationalities · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWe aimed to investigate the anti-angiogenic properties of miR-155 via in vitro and in vivo studies.

methodsmiR-155 was knocked down using lentivirus-mediated RNA interference. The proliferation, migration, and tube formation of human retinal microvascular endothelial cells (HRMECs) were measured using BrdU, Transwell, and Matrigel assays, respectively. An oxygen-induced retinopathy (OIR) model was induced using neonatal C57BL/6J pups. Anti-miR-155 was intravitreally injected on postnatal day 12, and the retinal non-perfused areas and extent of neovascularization were measured on postnatal day 18 using transcardiovascular fluorescein isothiocyanate (FITC)-dextran perfusion and retina sections. A laser-induced choroidal neovascularization (CNV) model was induced in adult C57BL/6J mice. To evaluate the leakage areas, fundus fluorescein angiography was performed on day 14 after anti-miR-155 intravitreal injection. The neovascularization area of the CNV model was also examined in confocal and retina section studies. The expression levels of SHIP1 and p-Akt (Thr308, Ser473, and Thr450) were evaluated both in vitro and in vivo.

resultsThe expression of miR-155 was elevated in HRMECs after treatment with vascular endothelial growth factor (VEGF) and in neovascularized mouse model retinas. Anti-miR-155 lentivirus reduced the VEGF-induced proliferation, migration, and tube formation abilities of HRMECs. Anti-miR-155 attenuated retinal neovascularization in in vivo CNV and OIR models. In VEGF-treated HRMECs and retina neovascularization models, p-Akt (Ser473) was significantly upregulated, while SHIP1 was downregulated. Conversely, the inhibition of miR-155 restored the expression of SHIP1 and reduced the phosphorylation of effectors in the Akt (Ser473) signaling pathway.

conclusionsThe results revealed that the downregulation of miR-155 attenuated retinal neovascularization via the phosphatidylinositol 3-kinase (PI3K)/Akt pathway.

Indexed as

AnimalsAnimals, NewbornCell MovementCell ProliferationChoroidal NeovascularizationEndothelial CellsFluorescein AngiographyGene Expression RegulationGenetic VectorsHumansInositol Polyphosphate 5-PhosphatasesIntravitreal InjectionsLentivirusMiceMice, Inbred C57BLMicroRNAsInositol Polyphosphate 5-PhosphatasesINPP5D protein, humanInpp5d protein, mouseMicroRNAsMIRN155 microRNA, humanOligonucleotidesPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID26539029
PMCPMC4605754
OpenAlexW2209281541

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.