Related Experiment Video

Updated: Oct 13, 2025

Loss-of-Function Approach in the Embryonic Chick Retina by Using Tol2 Transposon-Mediated Transgenic Expression of Artificial microRNAs
06:58

Loss-of-Function Approach in the Embryonic Chick Retina by Using Tol2 Transposon-Mediated Transgenic Expression of Artificial microRNAs

Published on: May 18, 2022

1.2K

Maternally expressed gene 3 regulates retinal neovascularization in retinopathy of prematurity

Yu Di1, Yue Wang1, Yue-Xia Wang1

  • 1Department of Ophthalmology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.

Neural Regeneration Research
|November 16, 2021
PubMed

Insights

Maternally expressed gene 3 (MEG3) overexpression inhibits retinal neovascularization in a mouse model of oxygen-induced retinopathy. This finding suggests MEG3 lentivirus could treat retinopathy of prematurity.

Area of Science:

  • Ophthalmology
  • Genetics
  • Molecular Biology

Background:

  • Oxygen-induced retinopathy (OIR) mouse model is crucial for studying retinal neovascularization diseases like retinopathy of prematurity.
  • Maternally expressed gene 3 (MEG3) shows inhibitory effects in diabetic retinopathy.

Purpose of the Study:

  • To investigate the role and mechanism of MEG3 overexpression in OIR mice.
  • To evaluate the potential of MEG3 lentivirus for treating retinopathy of prematurity.

Main Methods:

  • Establishing an oxygen-induced retinopathy mouse model.
  • Overexpressing MEG3 using lentivirus in OIR mice.
  • Analyzing the expression of key signaling molecules and inflammatory factors.

Main Results:

  • MEG3 overexpression significantly inhibited retinal neovascularization in OIR mice.
  • MEG3 down-regulated the expression of phosphoinositide 3-kinase, serine/threonine kinase, vascular endothelial growth factor, and pro-inflammatory factors.
  • MEG3 overexpression demonstrated therapeutic potential in the OIR model.

Conclusions:

  • MEG3 overexpression effectively suppresses retinal neovascularization in OIR by modulating specific molecular pathways.
  • MEG3 lentivirus represents a promising therapeutic strategy for retinopathy of prematurity.
Keywords:
long noncoding RNAmaternally expressed gene 3neurodevelopmentoxygen-induced retinopathyphosphoinositide 3-kinaseretinal neovascularizationretinopathy of prematurityserine/threonine kinasevascular endothelial growth factor

More Related Videos

Whole Mount Immunofluorescent Staining of the Neonatal Mouse Retina to Investigate Angiogenesis In vivo08:47

Whole Mount Immunofluorescent Staining of the Neonatal Mouse Retina to Investigate Angiogenesis In vivo

Published on: July 9, 2013

46.3K
Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model10:32

Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model

Published on: April 2, 2021

3.8K

Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.2K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.9K