April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Amyloid β Enhances Migration Of Endothelial Progenitor Cells Via Upregulation Of CX3CR1
Author Affiliations & Notes
  • Jiying Wang
    Ophthalmology & Visual Sci, Tokyo Medical & Dental Univ, Tokyo, Japan
  • Kyoko Ohno-Matsui
    Ophthalmology & Visual Sci, Tokyo Medical & Dental Univ, Tokyo, Japan
  • Takeshi Yoshida
    Ophthalmology & Visual Sci, Tokyo Medical & Dental Univ, Tokyo, Japan
  • Noriaki Shimada
    Ophthalmology & Visual Sci, Tokyo Medical & Dental Univ, Tokyo, Japan
  • Manabu Mochizuki
    Ophthalmology & Visual Sci, Tokyo Medical & Dental Univ, Tokyo, Japan
  • Ikuo Morita
    Cellular Physiological Chemistry, Tokyo, Japan
  • Footnotes
    Commercial Relationships  Jiying Wang, None; Kyoko Ohno-Matsui, None; Takeshi Yoshida, None; Noriaki Shimada, None; Manabu Mochizuki, None; Ikuo Morita, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 3194. doi:
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      Jiying Wang, Kyoko Ohno-Matsui, Takeshi Yoshida, Noriaki Shimada, Manabu Mochizuki, Ikuo Morita; Amyloid β Enhances Migration Of Endothelial Progenitor Cells Via Upregulation Of CX3CR1. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3194.

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

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Abstract

Purpose: : Amyloid β (Aβ) is accumulated within drusen and reportedly critical for pathogenesis of age-related macular degeneration (AMD). Endothelial progenitor cells (EPC) contributed to the development of CNV via matrix degrading enzyme; cathepsin L. We previously reported that Aβ enhanced the production of pro-inflammatory cytokines in EPC (ARVO2010). In the present study we investigated the molecular mechanism of the recruitment of EPC to subretinal space secondary to Aβ accumulation.

Methods: : EPC were isolated from the cultivation of mononuclear cells in human cord blood from healthy newborns. EPC were stimulated by Aβ or pro-inflammatory cytokines (IL-1β, TNF-α) . The mRNA expression and protein production of fractalkine and its receptor; CX3CR1 was analyzed by real-time PCR and western blot. Migratory activity was measured by Boyden chamber assay. The role of CX3CR1 in choroidal neovascularization (CNV) development was analyzed using laser-induced CNV model.

Results: : IL-1β, TNF-α significantly increased the expression and protein production of fractalkine. Aβ treatment induced a significant increase of CX3CR1 expression and protein production. In Boyden chamber assay, fractalkine caused a remarkable migration of EPC in a dose-dependent manner. Fractalkine-induced migration of EPC was significantly enhanced in Aβ-treated EPC compared to non-treated EPC. Laser-induced CNV was significantly suppressed in CX3CR1-/- mice compared to wild type mice.

Conclusions: : These results suggest the possibility that Aβ causes the migration of EPC to the area of drusen via up-regulation of CX3CR1 as well as cytokine-induced up-regulation of fractalkine. This phenomenon might be an important process for the CNV development in AMD.

Keywords: age-related macular degeneration • choroid: neovascularization • pathology: experimental 
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