Endothelial progenitor cells proliferated via MEK-dependent p42 MAPK signaling pathway

摘要: Endothelial progenitor cells (EPCs) clinical applications have been well reported. However, due to low number of EPCs that could be isolated, expansion study became one the main focuses. Some optimized mediums culture were currently available. proliferation signaling pathway is not clearly disclosed yet. Peripheral blood was collected from eight healthy subjects, followed by mononuclear (MNCs) isolation. MNCs then prepared and cultured for 2 days. After that, non-adherent harvested further 3 Resulted colony-forming unit (CFU)-Hill colonies documented enumerated under an inverted light microscope. To detect membrane markers, immunofluorescence performed CD34, VEGFR-2, CD133. Cell documentation conducted a fluorescence check cell proliferation, XTT Proliferation Assay Kit used according kit insert. possible activation p44/42 MAPK, western blot MAPK phosphorylated MAPK. All visualized bands captured quantified. Our results showed markers (CD34, CD133 VEGFR-2) detected in days culture. From assay CFU enumeration results, we found proliferated significantly (p = 0.012) with addition supplement. Phosphorylated-p42 expression treated supplement higher than without treatment. Significant inhibition p42 phosphorylation U0126 observed 0.012). By pretreatment U0126, viable CFUs decreased MEK-dependent might play important role proliferation.