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Retinal neovascular markers in retinopathy of prematurity: aetiological implications
P E North1, D C Anthony, T L Young
1Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA. northpaulae@uams.edu
Insights
Glucose transporter GLUT1 is retained in retinopathy of prematurity (ROP) neovascularization, unlike in diabetic retinopathy. ROP also lacks Lewis Y antigen, distinguishing it from juvenile hemangioma.
Area of Science:
- Ophthalmology
- Vascular Biology
- Developmental Biology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of blindness in premature infants.
- The neovasculature in ROP shares some characteristics with other neovascular disorders, but its specific molecular profile is not fully understood.
- Understanding the unique features of ROP neovascularization is crucial for developing targeted therapies.
Observation:
- This study investigated the expression of glucose transporter GLUT1 and Lewis Y antigen in the neovasculature of ROP.
- Immunoreactivity for GLUT1 was assessed in a human eye with stage 3 ROP and compared to a control eye.
- Lewis Y antigen expression was also evaluated in ROP and compared to juvenile hemangioma.
Findings:
- The neovasculature in ROP, both intraretinal and preretinal, demonstrated positive immunoreactivity for GLUT1.
- In contrast, Lewis Y antigen was negative in the ROP neovasculature.
- Normal retinal vessels in the control eye also showed GLUT1 immunoreactivity.
Implications:
- The retention of GLUT1 expression in ROP neovascularization differentiates it from proliferative diabetic retinopathy, where GLUT1 is lost.
- The absence of Lewis Y antigen in ROP distinguishes it from juvenile hemangioma, another neovascular disorder.
- These findings highlight distinct molecular signatures of neovascularization in different conditions, aiding in diagnosis and therapeutic strategies.
Aim:
(1) To determine if expression of the blood-tissue barrier associated glucose transporter GLUT1 is preserved by the neovasculature of retinopathy of prematurity (ROP), in contrast with the reported loss of GLUT1 expression in preretinal vessels of proliferative diabetic retinopathy. (2) To compare the vascular immunophenotype of ROP to juvenile haemangioma, another perinatal neovascular disorder that has recently been shown to express placental type vascular antigens, including GLUT1 and Lewis Y antigen.
Methods:
A retrospective case report was carried out. Immunoreactivities for GLUT1 and Lewis Y antigen were assessed in a human eye with stage 3 ROP and compared with those in a control (paediatric) eye. The presence or absence of endothelial GLUT1 and Lewis Y immunoreactivity was determined in preretinal and intraretinal vessels.
Results:
Immunoreactivity was positive for GLUT1 and negative for Lewis Y in the intraretinal and preretinal neovasculature of the ROP affected eye and in the normal retinal vessels of the control eye.
Conclusions:
Retention of immunoreactivity for GLUT1 distinguishes ROP from proliferative diabetic retinopathy. Furthermore, absence of Lewis Y antigen co-expression distinguishes ROP from juvenile haemangioma, a perinatal form of GLUT1 positive neovascularisation that has recently been linked to placental vasculature.
