April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Tissue Factor Regulates Fibroblast Growth Factor-2-Induced Angiogenesis in Retinoblastoma
Author Affiliations & Notes
  • M. S. Jeong
    Opthalomology, Seoul National University hospital, Seoul, Republic of Korea
  • J. H. Kim
    Opthalomology, Seoul National University Hospital, Seoul, Republic of Korea
  • K.-W. Kim
    College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea
  • Y. S. Yu
    Opthalomology, Seoul National University Hospital, Seoul, Republic of Korea
  • J. H. Kim
    Opthalomology, Seoul National University Hospital, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships  M.S. Jeong, None; J.H. Kim, None; K.-W. Kim, None; Y.S. Yu, None; J.H. Kim, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 53. doi:
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      M. S. Jeong, J. H. Kim, K.-W. Kim, Y. S. Yu, J. H. Kim; Tissue Factor Regulates Fibroblast Growth Factor-2-Induced Angiogenesis in Retinoblastoma. Invest. Ophthalmol. Vis. Sci. 2010;51(13):53.

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

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Abstract

Purpose: : To investigate whether tissue factor (TF) regulates fibroblast growth factor (FGF)-2-induced angiogenesis in retinoblastoma.

Methods: : In an experimental model of retinoblastoma, immunofluorescence staining for TF and CD31 as an endothelial cell maker was performed. With treatment of FGF-2 (10 ng/ml), TF expression in human umbilical vein endothelial cells (HUVECs) was measured by Western blotting. To confirm the role of TF in tumor angiogenesis in retinoblastoma, anti-angiogenic activity of TF pathway inhibitor (TFPI) was evaluated by FGF-2-induced proliferation, migration and in vitro tube formation assay of HUVECs. In addition, inhibition of ERK-1/2 phosphorylation by TFPI was measured by Western blot analysis.

Results: : TF was highly expressed on vascular endothelial cells of retinoblastoma, co-localized with CD31. With FGF-2-induced proliferation of HUVECs, TF expression was significantly up-regulated. Interestingly, TFPI effectively blocked FGF-2-induced proliferation, migration and in vitro tube formation of HUVECs, which was accompanied by inhibition of ERK-1/2 phosphorylation.

Conclusions: : Our results suggest that TF on tumor vessels of retinoblastoma could be involved in regulation of FGF-2 induced angiogenesis, which was mediated by ERK pathway.

Keywords: retinoblastoma • tumors • growth factors/growth factor receptors 
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