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Updated: Aug 17, 2026
Assessment and Characterization of Hyaloid Vessels in Mice
Published on: May 15, 2019
Persistent fetal ocular vasculature in mice deficient in bax and bak
Paul Hahn1, Tullia Lindsten, Michael Tolentino
1Departments of Medicine, Pathology, and Laboratory Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA.
Background:
The ocular fetal vasculature normally regresses by apoptosis but for unknown reasons fails to regress in the human disease persistent fetal vasculature.
Objective:
To investigate whether proapoptotic Bcl-2 members, Bax and Bak, are involved in fetal vasculature regression.
Methods:
Adult eyes from mice deficient in Bax and/or Bak were examined grossly and histologically for persistence of fetal vasculature. Vessels were identified by the presence of lumens and erythrocytes and by Factor VIII labeling. Eyes from postnatal day 7 mice were processed for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) analysis to determine if deficiency of Bax and Bak results in defective developmental apoptosis.
Results:
Only bax(-/-)bak(-/-) eyes retained fetal vasculature into adulthood. This vasculature consisted of a hyaloid artery emerging from the optic nerve head and intravitreal and perilental vessels but not a pupillary membrane. At postnatal day 7, wild-type but not bax(-/-)bak(-/-) eyes had TUNEL-positive cells in the fetal vasculature.
Conclusions:
These data demonstrate that Bax and Bak serve overlapping functions in fetal vasculature regression, emphasizing the importance of apoptosis in developmental remodeling. Clinical Relevance Disruption of Bax and Bak results in persistent fetal vasculature in knockout mice, providing a model of the human disease persistent fetal vasculature to investigate its etiology and potential therapies.
Insights
Bax and Bak proteins are crucial for the regression of fetal vasculature through apoptosis. Their absence in mice leads to persistent fetal vasculature, a model for the human disease.
Area of Science:
- Ophthalmology
- Developmental Biology
- Molecular Biology
Background:
- Ocular fetal vasculature normally regresses via apoptosis.
- Persistent fetal vasculature (PFV) is a human disease where this regression fails.
- The underlying mechanisms of PFV are not fully understood.
Purpose of the Study:
- To investigate the role of proapoptotic Bcl-2 family members, Bax and Bak, in fetal vasculature regression.
- To determine if Bax and Bak are essential for the developmental apoptosis of ocular vasculature.
Main Methods:
- Examined adult eyes from mice genetically deficient in Bax and/or Bak for persistent fetal vasculature.
- Used Factor VIII labeling to identify blood vessels.
- Performed TUNEL analysis on postnatal day 7 mouse eyes to assess developmental apoptosis.
Main Results:
- Only mice lacking both Bax and Bak (bax(-/-)bak(-/-)) exhibited persistent fetal vasculature into adulthood.
- This persistent vasculature included hyaloid arteries and intravitreal/perilental vessels.
- Postnatal day 7 knockout eyes showed a lack of developmental apoptosis (TUNEL-positive cells) in the fetal vasculature compared to wild-type.
Conclusions:
- Bax and Bak have overlapping roles in the regression of fetal vasculature.
- Apoptosis, mediated by Bax and Bak, is vital for developmental vascular remodeling.
- Bax and Bak deficiency in mice creates a model for studying persistent fetal vasculature and potential treatments.
