Dysfunction of endothelial progenitor cells (EPCs) has been reported either in aging or diabetes, though the influence of an "old" environment on numerical and functional changes of diabetes associated EPCs is not known. We evaluated the effect of both aging and early stage of streptozotocin-induced diabetes on the number of bone marrow-derived CD117(+) progenitor cells, and on their differentiation in vitro toward EPCs. The phenotype of progenitor cells and the uptake of acetylated-low density lipoprotein (Ac-LDL) were evaluated after cell culture in VEGF, FGF-1, and IGF-1 supplemented medium. Hyperglycemia similarly reduced the number of CD117(+) cells both in young and old mice. CD117(+) cells from young mice differentiated better than those from old animals "in vitro", with a greater reduction of CD117(+) cells and an higher increase of CD184(+)VEGFR-2(+) cells. In diabetic mice, in vitro CD117(+) cells differentiation was significantly reduced in young animals. Diabetes did not impact on the scarce differentiation of CD117(+) cells from old mice. Hyperglycemia reduced the uptake of acLDL by EPCs greatly in young than in old mice. These findings indicate that part of the EPCs functional alterations induced by hyperglicemia in young mice are observed in normal aged mice.
- Journal Article