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Updated: Apr 21, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Reduced β‑2‑glycoprotein І inhibits hypoxia‑induced retinal angiogenesis in neonatal mice through the vascular
Hongyan Liu1, Saijun Zhou1, Gareth Denyer2
12011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Key Laboratory of Hormones and Development (Ministry of Health), Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, P.R. China.
Abstract:
β‑2‑glycoprotein I (β2GPI), also known as apolipoprotein H, is a phospholipid‑binding plasma protein consisting of five homologous repeated units. β2GPI downregulates vascular endothelial growth factor (VEGF) signaling pathways and inhibits angiogenesis in vitro. However, the in vivo roles and effectors of reduced β2GPI and β2GPI in retinal angiogenesis are still not fully understood. In this study, an oxygen‑induced retinopathy model was used to investigate the effects of reduced β2GPI and β2GPI, and to monitor the expression of VEGF, VEGF receptor (VEGFR) 1, VEGFR‑2 and hypoxia‑inducible factor 1 (HIF‑1) mRNA and the phosphorylation of extracellular signal‑regulated kinase (ERK) and Akt. The data showed that both β2GPI and reduced β2GPI inhibited retinal angiogenesis and suppressed the expression of VEGF, VEGFR‑1, VEGFR‑2, HIF‑1, phosphorylated- (p‑) ERK and p‑Akt. The effects of reduced β2GPI were significantly stronger than those of β2GPI. In conclusion, this study showed that β2GPI and reduced β2GPI could inhibit retinal angiogenesis by downregulating the expression of VEGF and its downstream targets. This suggests that β2GPI and reduced β2GPI may have potential anti‑angiogenic activity in vivo.
Insights
Beta-2-glycoprotein I (β2GPI) and its reduced form inhibit retinal angiogenesis by downregulating VEGF signaling. Reduced β2GPI demonstrated stronger anti-angiogenic effects in vivo.
Area of Science:
- Ophthalmology
- Vascular Biology
- Biochemistry
Background:
- Beta-2-glycoprotein I (β2GPI), or apolipoprotein H, is a plasma protein that binds phospholipids.
- β2GPI is known to inhibit angiogenesis in vitro by downregulating vascular endothelial growth factor (VEGF) signaling.
- The in vivo role of β2GPI and its reduced form in retinal angiogenesis remains unclear.
Purpose of the Study:
- To investigate the effects of β2GPI and reduced β2GPI on retinal angiogenesis in vivo.
- To examine the expression of key angiogenic factors including VEGF, VEGFR-1, VEGFR-2, and HIF-1 mRNA.
- To assess the phosphorylation status of ERK and Akt signaling pathways.
Main Methods:
- Utilized an oxygen-induced retinopathy model in vivo.
- Monitored retinal angiogenesis.
- Measured mRNA expression of VEGF, VEGFR-1, VEGFR-2, and HIF-1.
- Assessed phosphorylation of ERK and Akt.
Main Results:
- Both β2GPI and reduced β2GPI significantly inhibited retinal angiogenesis.
- Expression of VEGF, VEGFR-1, VEGFR-2, HIF-1, phosphorylated-ERK (p-ERK), and phosphorylated-Akt (p-Akt) were suppressed.
- The inhibitory effects of reduced β2GPI were more pronounced than those of native β2GPI.
Conclusions:
- β2GPI and its reduced form inhibit retinal angiogenesis in vivo.
- This inhibition occurs through the downregulation of VEGF and its downstream signaling pathways.
- β2GPI and reduced β2GPI show potential as therapeutic agents for anti-angiogenic therapy in ocular diseases.
