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Regulation of Angiogenesis and Blood Supply

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 hydroxylase and factor...

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Related Experiment Video

Updated: May 28, 2026

Nitroreductase/Metronidazole-Mediated Ablation and a MATLAB Platform (RpEGEN) for Studying Regeneration of the Zebrafish Retinal Pigment Epithelium

Nitroreductase/Metronidazole-Mediated Ablation and a MATLAB Platform (RpEGEN) for Studying Regeneration of the Zebrafish Retinal Pigment Epithelium

Published on: March 2, 2022

Zeb2 Controls Retinal Physiological and Pathological Angiogenesis by Regulating Astrocyte Proliferation and

Jing Liu¹, Yanan Guo¹, Kangjian Xiang¹

¹State Key Laboratory of Ophthalmology, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.

Cell Proliferation

|May 26, 2026

Summary

Zeb2 regulates retinal blood vessel growth in astrocytes. Loss of Zeb2 causes abnormal development and worsens disease, suggesting it's a therapeutic target for proliferative retinopathies.

Keywords:

Zeb2 neurotoxic astrocyte oxygen‐induced retinopathy proliferation retinal astrocyte retinopathy of prematurity

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Area of Science:

Neuroscience
Ophthalmology
Molecular Biology

Background:

Retinal angiogenesis involves astrocyte-endothelial cell (EC) interactions.
The transcriptional regulation of this neurovascular crosstalk is not well understood.

Purpose of the Study:

To define Zeb2's role in retinal astrocyte function.
To investigate Zeb2's modulation of developmental and pathological retinal angiogenesis.

Main Methods:

Conditional Zeb2 ablation in retinal astrocytes.
Analysis of vascular growth in developmental models and oxygen-induced retinopathy.
Transcriptional profiling and mechanistic studies.

Main Results:

Zeb2 deficiency in astrocytes enhanced proliferation, migration, and VEGFA upregulation, leading to excessive vascular growth.
Zeb2 inactivation worsened pathological neovascularization and impaired reparative revascularization in retinopathy.
Zeb2 inhibited A1 astrocyte identity, reducing inflammation and key signaling pathways (Plxnd1, Nrf2, FGF2).

Conclusions:

Zeb2 is an oxygen-sensitive regulator of astrocyte function.
Zeb2 differentially controls physiological and pathological retinal angiogenesis.
Zeb2 presents a potential therapeutic target for proliferative retinopathies.