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F. Scotti, A. Maestroni, S. Maestroni, U. Introini, M. Setaccioli, P. Rama, F. Bandello, M. Lorenzi, G. Zerbini; Decreased Clonogenic Capacity of Endothelial Progenitor Cells (EPCs) in Age Related Macular Degeneration (AMD). Invest. Ophthalmol. Vis. Sci. 2010;51(13):2667.
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The major cause of severe vision loss in AMD is choroidal neovascularization (CNV). The aim of this ongoing study is to learn whether active CNV is accompanied by changes in circulating EPC.
The study of AMD patients with new-onset CNV scheduled for intravitreal ranibizumab (IVR), is enabling us to observe in the same patient the relationship of EPC to evolving stages of CNV. To date, we completed data collection in 11 AMD subjects (6F/5M, age 74±8 yrs) undergoing the recommended cycle of IVR (3 monthly injections). Blood samples were obtained at baseline, and at 4, 30, and 120 days after the first injection. The 120 days sample was collected 30 days after the final IVR. Nine subjects matched for age (69±6 yrs) and gender (5F/4M) but without AMD provided control baseline data. We measured (i) the number of circulating EPCs (CD45dim, CD34+, VEGFR-2+) by flow cytometry; (ii) their clonogenic capacity by the Hill’s assay; and (iii) the plasma levels of VEGF and SDF-1, the two cytokines known to mobilize EPC, by ELISA.
Clinical improvement occurred in 6 of the 11 patients. At baseline, the number of circulating EPC and the VEGF and SDF-1 plasma levels were similar in AMD patients and controls. In a subset of patients, the number of EPC responded to IVR but was not correlated with the clinical response. The striking observation is the much lower clonogenic capacity of EPCs obtained at baseline from AMD patients when compared to controls (1.97±1.14 EPC colonies /106 mononuclear cells, vs 5.06±1.42 in controls, mean±SD, P=0.0001). At 120 days, the clonogenic capacity of EPCs from patients who did not improve clinically remained low (1.90±1.19 vs1.85±0.89 at baseline); whereas that of the EPCs from patients who did not improve appeared to increase (2.83±1.53 vs 2.07±1.40 at baseline).
. The decreased clonogenic capacity of EPCs from AMD patients may reflect the increased cardiovascular risk that is being reported in this population. However, its apparent association with active CNV may be revealing that CNV signals to the function of circulating EPCs.
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