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Paul Hahn, PhD; Tullia Lindsten, MD, PhD; Michael Tolentino, MD; Craig B. Thompson, MD; Jean Bennett, MD, PhD; Joshua L. Dunaief, MD, PhD

Arch Ophthalmol. 2005;123:797-802.

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.

Author Affiliations: F.M. Kirby Center for Molecular Ophthalmology, Scheie Eye Institute (Drs Hahn, Tolentino, Bennett, and Dunaief); Departments of Medicine, Pathology, and Laboratory Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia (Drs Lindsten and Thompson).

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