May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
AQ4N, a Cytotoxic Prodrug, Inhibits Proliferation and VEGF Secretion in Retinal Cells
Author Affiliations & Notes
  • S. Raghava
    University of Nebraska Medical Center, Omaha,, NE
    Pharmaceutical Sciences,
  • U.B. Kompella
    University of Nebraska Medical Center, Omaha,, NE
    Pharmaceutical Sciences and Ophthalomology,
  • Footnotes
    Commercial Relationships  S. Raghava, None; U.B. Kompella, None.
  • Footnotes
    Support  Novacea
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2884. doi:
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      S. Raghava, U.B. Kompella; AQ4N, a Cytotoxic Prodrug, Inhibits Proliferation and VEGF Secretion in Retinal Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2884.

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

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Abstract

Purpose: : AQ4N is an anticancer prodrug, which is bioreduced to the active DNA intercalating topoisomerase II inhibitor, AQ4, under hypoxia. Thus, AQ4N can exhibit selective cytotoxicity in hypoxic regions. The purpose of this study was to assess whether AQ4N and AQ4 exhibit anti–proliferative effect in ocular endothelial cells, the proliferation and neovascularization of which is implicated in retinal disorders such as diabetic retinopathy and age–related macular degeneration. Further, it was the purpose of this study to assess the effects of these agents on VEGF secretion from retinal pigment epithelial (RPE) cells, a key source of retinal VEGF.

Methods: : The cytotoxicity and antiproliferative activity were assessed in RF/6A (a monkey choroid/retinal endothelial cell line) and ARPE–19 (a human RPE cell line) cells, while VEGF secretion was assessed in ARPE–19 cells. All the studies were carried out after exposing cell monolayers to treatment solutions in 96 well plates for a duration of 12 hours under normoxic (21% O2) or hypoxic (1% O2) culture conditions. The cytotoxicity, anti–proliferative activity and anti–VEGF activity were assessed by MTT assay, BrDU assay and VEGF ELISA, respectively.

Results: : AQ4N did not exhibit cytotoxicity up to a concentration of 1 mM, while AQ4 showed significant cytotoxicity at a concentration of 0.1 mM in both the cell lines, under normoxia as well as hypoxia. AQ4N did not show antiproliferative activity up to a concentration of 20 µM in both the cell lines; however, AQ4 reduced the percentage of proliferating cells to zero at a concentration of 20 µM in both the cell lines. Treatment of ARPE 19 cells with 20 µM AQ4N did not reduce VEGF secretion by ARPE 19 cells, while 20 µM AQ4 reduced VEGF secretion by 50% under normoxic and hypoxic conditions. Hypoxia significantly increased the level of VEGF secretion by ARPE 19 cells as compared to normoxia controls.

Conclusions: : AQ4, the active drug, was found to be 10 times more cytotoxic than AQ4N, in both the cell lines. AQ4, but not AQ4N, has anti–proliferative activity in both ARPE 19 and RF/6A cell lines and reduced secretion of VEGF in ARPE–19 cells. Identification of a prodrug/drug concentration that inhibits endothelial cell proliferation and VEGF secretion from RPE cells without any toxic effects in RPE cells would be useful for neovascular disorders of the eye.

Keywords: age-related macular degeneration • choroid: neovascularization • hypoxia 
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