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(OR15-03-26) Maternal Supplementation of Lutein Improved Retinal Vessel Morphology in Neonatal Isx-/-/Bco2-/- Mice with Retinopathy of Prematurity

Monday, July 27, 2026
8:54 AM - 9:06 AM ET
Location: National Harbor 4-5

    Presenting Author(s)

  • Zhi Zheng, Masters degree (she/her/hers)

    Doctoral Student
    The University of Alabama
    Tuscaloosa, Alabama, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • NM

    Nolan McKibben

    The University of Alabama, United States

  • JW

    Jun Wang

    The University of Alabama, United States

  • SA

    Sayma Alam

    The University of Alabama, United States

  • LT

    Libo Tan

    The University of Alabama, United States

Disclosure(s):
Zhi Zheng, Masters degree: No relevant financial relationship(s) with ineligible companies to disclose.
Objectives: Retinopathy of prematurity (ROP) is an eye disease in premature infants characterized by abnormal retinal blood vessel growth. Lutein, a dietary antioxidant and a major component of macular pigments, may help ameliorate ROP. Our previous study showed that oral lutein improved retinal artery tortuosity, capillary density, vessel diameter, astrocyte distribution, and neuronal cell number in neonatal Sprague-Dawley (SD) rats with ROP. However, lutein was administered only postnatally, whereas maternal lutein supplementation may provide a safer and more sustained exposure for vulnerable infants. Moreover, SD rats exhibit much lower ocular lutein concentrations than humans due to active beta-carotene oxygenase 2 (BCO2). Therefore, this study aimed to examine the effects of maternal lutein supplementation on ROP progression in neonatal Isx-/-/Bco2-/- mice.

Methods: From embryonic day 0 to postnatal day 21, mouse dams were randomly assigned to either a lutein fortified diet or a control diet. At P7 and P8, ROP was induced to half of the pups in each group by injection of KRN 633, a VEGF receptor inhibitor that induces abnormal retinal vascular growth. At P22, pups were euthanized and retinal vasculature, including artery tortuosity, vessel diameter, and capillary density, as well as astrocytes and neuronal cells were analyzed via immunohistochemistry.

Results: Neonatal ROP mice exhibited increased arterial tortuosity, larger retinal vessel diameters, and higher capillary density, along with a reduced number of neuronal cells. These abnormalities were significantly improved to levels comparable to the control group in ROP mice exposed to maternal lutein supplementation.

Conclusions: Maternal lutein supplementation improved retinal vascular morphology in neonatal Isx-/-/Bco2-/- mice with ROP. These promising findings support future clinical studies investigating maternal lutein supplementation as a potential strategy for delivering lutein to benefit preterm infants at risk for ROP.

Funding Sources: Sigma Xi Grants in Aid of Research