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Updated: Jun 27, 2026
Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
Published on: June 23, 2014
Limited hyperoxia-induced proliferative retinopathy: A model of persistent retinal vascular dysfunction, preretinal
Thomas Tedeschi1, Kendal Lee1, Wei Zhu1,2
1Department of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States of America.
Insights
This study details the limited hyperoxia induced proliferative retinopathy (L-HIPR) model, revealing persistent hyaloidal vessels and retinal changes. Findings suggest these vessels may aid inner retinal development in this retinopathy of prematurity model.
Area of Science:
- Ophthalmology
- Developmental Biology
- Animal Models
Background:
- Retinopathy of prematurity (ROP) is a primary cause of childhood blindness.
- The limited hyperoxia induced proliferative retinopathy (L-HIPR) model offers insights into ROP and persistent fetal vasculature.
- Detailed pathological changes in the L-HIPR model require further elucidation.
Purpose of the Study:
- To comprehensively analyze the pathological changes in the L-HIPR mouse model.
- To investigate the role of persistent hyaloidal vessels in retinal development within the L-HIPR model.
- To characterize vitreoretinal pathology, including fibrosis and vascular abnormalities.
Main Methods:
- C57BL/6J mice were exposed to 65% oxygen from birth to postnatal day 7.
- Ocular tissues were examined from postnatal day 12 to 30.
- Histology, immunohistochemistry, and morphometric analyses were employed to assess vascular development, inflammation, fibrosis, and pericyte coverage.
Main Results:
- Persistent hyaloidal vessels were observed up to postnatal day 30, invading the retina.
- Retinal distortion and thinning were noted, alongside delayed and abnormal vascular development.
- The L-HIPR model exhibited retinal inflammation, pericyte loss, and preretinal fibrosis.
Conclusions:
- The L-HIPR model demonstrates significant vitreoretinal pathological changes, including fibrosis and persistent hyaloidal vessels into adulthood.
- Persistent hyaloidal vessels may act as a rescue mechanism for inner retinal development.
- Further research is warranted to explore the implications of hyaloidal vessel migration in retinal development.
Background:
Retinopathy of prematurity (ROP) remains the leading cause for blindness in children. Limited hyperoxia induced proliferative retinopathy (L-HIPR) was recently introduced as a potential animal model for ROP and persistent fetal vasculature; however, the detailed pathological changes remain unclear.
Methods:
To model L-HIPR, we placed C57BL/6J mice in 65% oxygen from birth to post-natal day 7 (P7). We examined eyes at intervals between P12 and P30. Retinal morphometry, thickness, and preretinal fibrosis were quantified at different time points on histological sections stained with hematoxylin and eosin (H&E) and Masson Trichrome, respectively. Vascular development, angiogenesis, inflammation, and pericyte coverage were analyzed using immunohistochemistry staining in retinal flat mounts and cross sections.
Results:
In L-HIPR, the hyaloidal vessels persisted until the latest time point in this study, P30 and began to invaginate the peripheral then central retina starting at P12. Central retinal distortion was noted beginning at P17, while the peripheral retina demonstrated a trend of thinning from P12 to P30. We found that L-HIPR was associated with delayed and abnormal retinal vascular development with subsequent retinal inflammation, pericyte loss and preretinal fibrosis.
Conclusion:
Our study presents a detailed analysis of the L-HIPR animal model demonstrating vitreoretinal pathologic changes, preretinal fibrosis and persistent hyaloidal vessels into adulthood. Based on our findings, we suggest that the persistence and peculiar stepwise migration of the hyaloidal vessels into the retina may provide a potential rescue mechanism for inner retinal development that deserves further study.
