January 1995
Volume 36, Issue 1
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Articles  |   January 1995
Vitamin D inhibits angiogenesis in transgenic murine retinoblastoma.
Author Affiliations
  • M T Shokravi
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston.
  • D M Marcus
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston.
  • J Alroy
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston.
  • K Egan
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston.
  • M A Saornil
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston.
  • D M Albert
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston.
Investigative Ophthalmology & Visual Science January 1995, Vol.36, 83-87. doi:
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    • Get Citation

      M T Shokravi, D M Marcus, J Alroy, K Egan, M A Saornil, D M Albert; Vitamin D inhibits angiogenesis in transgenic murine retinoblastoma.. Invest. Ophthalmol. Vis. Sci. 1995;36(1):83-87.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: Vitamin D compounds have been shown to inhibit tumor growth in a transgenic retinoblastoma murine model. The mechanism of action has not been defined clearly, although an antiangiogenic action has been proposed. METHODS: Transgenic retinoblastoma mice received high (0.05 microgram) and low (0.025 microgram) doses of vitamin D3 by intraperitoneal injection 5 times per week for 5 weeks. Control animals were injected with mineral oil vehicle alone. At 5 months of age, the animals were killed and eyes were enucleated and processed for light microscopy. Paraffin-embedded sections were stained with an immunoperoxidase stain (GS-1) specific for mammalian vascular endothelium. Sections were graded by a single masked reviewer, and intraobserver reliability was assessed. Mean vessel counts were made for each group. RESULTS: The high-dose group had the lowest mean vessel count (8.5), followed by the low-dose group (10.1). The control group had the highest mean vessel count (14.1). Vitamin D-treated animals (high- and low-dose groups combined) had significantly fewer vessels P = 0.001) than untreated controls. CONCLUSIONS: These results support the hypothesis that inhibition of angiogenesis is a mechanism of action for vitamin D in the transgenic retinoblastoma mouse model.

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