April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Foxc1 Is Required for Corneal Avascularity
Author Affiliations & Notes
  • Seung Woon Seo
    FCVRI, Northwestern University, Chicago, Illinois
  • Tsutomu Kume
    FCVRI, Northwestern University, Chicago, Illinois
  • Footnotes
    Commercial Relationships  Seung Woon Seo, None; Tsutomu Kume, None
  • Footnotes
    Support  NIH Grant EY019484
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 6411. doi:
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      Seung Woon Seo, Tsutomu Kume; Foxc1 Is Required for Corneal Avascularity. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6411.

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

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Neural crest-derived cells (NCC) give rise to the stroma and endothelium of the cornea, an avascular organ whose transparency is critical for vision. However, the basic mechanisms of how pro-angiogenic and anti-angiogenic factors are regulated in the corneal stroma remain unknown. Mutations in human FOXC1 are associated with autosomal-dominant Axenfeld-Rieger Syndrome. In this study, we investigate the NCC-specific roles of Foxc1 in corneal avascularity.


Conditional mutant mice for Foxc1 were generated by crossing Foxc1F/F mice with Wnt1-Cre mice to make tissue-specific deletion of Foxc1 specifically in the neural crest lineage. Corneal flat mounts in NCC-specific Foxc1 mutant embryos and adult mice were performed to analyze the blood and lymphatic vessel formation using CD31 and LYVE1 antibodies, respectively. In alkali-burn induced cornea neovascularization (CNV) model, VEGF inhibitor (SU5416; 25 mg/kg body weight) was i.p. injected daily to control and mutant mice for 7 days, and the effects of the VEGF inhibitor on CNV were subsequently examined by corneal flat mounts.


NCC-specific Foxc1 mutants exhibit CNV (E14.5 to E15.5). NCC-specific Foxc1 mutants also show corneal lymphangiogenesis (E17.5 to E18.0). In the alkali-burn model without VEGF inhibition, corneas of adult Foxc1+/- and NCC-specific Foxc1F/+ mutant mice have increased CNV and lymphangiogenesis, compared with those of wild-type and control mice, respectively. By contrast, CNV and lymphangiogenesis were significantly reduced in corneas of adult Foxc1+/- and NCC-specific Foxc1F/+ mutant mice by treatment of the VEGF inhibitor.


The cell-autonomous function of Foxc1 in the neural crest is essential for inhibition of vascular formation in the cornea.  

Keywords: cornea: stroma and keratocytes • anterior segment • transcription factors 

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