April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
The Role of activin A in Angiogenesis
Author Affiliations & Notes
  • Kyoko Maeshima
    Ophthalmology, Gunma University Sch of Med, Maebashi, Japan
    Cell physiology, Institute for Molecular and Cellular Regulation, Maebashi, Japan
  • Itaru Kojima
    Cell physiology, Institute for Molecular and Cellular Regulation, Maebashi, Japan
  • Shoji Kishi
    Ophthalmology, Gunma University Sch of Med, Maebashi, Japan
  • Footnotes
    Commercial Relationships  Kyoko Maeshima, None; Itaru Kojima, None; Shoji Kishi, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4839. doi:
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      Kyoko Maeshima, Itaru Kojima, Shoji Kishi; The Role of activin A in Angiogenesis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4839.

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

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Purpose: : Activin A, a member of the TGF-beta superfamily, regulates cell proliferation and differentiation in various organs. Activin A has been reported to be involved in the formation of proliferative membrane and angiogenesis in proliferative vitreoretinal diseases. However, the precise mechanism by which activin modulates this process remains unclear. To clarify this issue, we examined the role of activin A in angiogenesis in vitro and in vivo.

Methods: : In vitro angiogenesis assay using human umbilical vein endothelial cells (HUVECs) was performed. HUVECs and fibroblasts were co-cultured in the collagen gel without cell-cell contact. The effect of activin A, follistatin (activin antagonist) and VEGF on tube formation was examined. The effect of activin A and follistatin on cell proliferation was also examined by MTT assay. In an in vivo laser-induced mouse choroidal neovasucularization (CNV) model, the expression of activin and its receptors was examined by immunostaining and the effect of an intravitreous injection of recombinant activin A on the size of CNV was evaluated.

Results: : Activin A potently inhibited tube formation in HUVECs cultured in gels and suppressed tubulogenic effect of VEGF. In contrast, follistatin significantly enhanced tube formation. Activin A significantly inhibited cell proliferation in HUVECs as assessed by the MTT assay. Activin A and its receptor were expressed in endothelial cells of CNV. The size of CNV treated by activin A was significantly smaller than that treated by PBS as a control.

Conclusions: : These findings suggest that activin A acts as a potent anti-angiogenic factor.

Keywords: growth factors/growth factor receptors • choroid: neovascularization 

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