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Jiying Wang, Kyoko Ohno-Matsui, Manabu Mochizuki, Ikuo Morita; Amyloid Beta Enhances Migration Of Endothelial Progenitor Cells Via Upregulation Of CX3CR1. Invest. Ophthalmol. Vis. Sci. 2012;53(14):1661.
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© ARVO (1962-2015); The Authors (2016-present)
Amyloid β (Aβ) is accumulated within drusen and reportedly critical for pathogenesis of age-related macular degeneration (AMD). We previously reported endothelial progenitor cells (EPC) contributed to the development of CNV (ARVO2011). In the present study we investigated the molecular mechanism of the recruitment of EPC to subretinal space secondary to Aβ accumulation.
EPC that isolated from human cord blood or peripheral blood of wild type and Cx3CR1-/- mice were stimulated by Aβ. CX3CR1 mRNA expression and protein production were analyzed by real-time PCR and western blot. Migratory activity was measured by Boyden chamber assay.
Aβ treatment induced a significant increase of CX3CR1 expression and protein production. In Boyden chamber assay, fractalkine caused a remarkable migration of human EPC and EPC isolated from wild type mice, but failed to induce migration of EPC from CX3CR1-/- mice. Aβ enhanced fractalkine-induced human and wild type EPC migration, but did not affect EPC from CX3CR1-/- mice.
These results suggest the possibility that Aβ causes the migration of EPC to the area of drusen specially via up-regulation of CX3CR1. This phenomenon might be an important process for the CNV development in AMD.
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