Background: Granulocyte-Colony Stimulating Factor (G-CSF) has been considered promising method to mobilize stem cells non-invasively and easily. But also, in controversy, proinflammatory and proatherogenic effect of G-CSF has been concerned. Presented putative underlying mechanism, G-CSF might stimulate C-reactive protein (CRP) in various degrees, via IL-6 in hepatocyte and aggravate endothelial dysfunction. But there have been few studies on the direct effect of G-CSF and G-CSF-CRP combination in endothelial dysfunction, because of too many compounding in human in vivo. Methods and Results: For analyzing the pure G-CSF effect on endothelial cell, human gastroepiploic artery and umbilical vein endothelial cells (HUVECs) were incubated with G-CSF (1, 10ng/ml) and recombinant CRP (3, 10 關g/ml). To assess the endothelial function, a wounding migration assay was performed. Time and dose dependently, G-CSF stimulated EC migration, whereas CRP reduced. When CRP and G-CSF were co-incubated, the CRP-mediated endothelial dysfunction was partially attenuated by G-CSF. The negative effect of CRP, however, was not reversed by G-CSF. Nitric oxide (NO) production and gene expression of endothelial NO synthase (eNOS) were also examined using a membrane-permeable NO detection reagent, diaminofluorescein-2-diacetate (DAF-2 DA) and RT-PCR. In the presence of CRP, NO production and eNOS gene expression were reduced whereas G-CSF increased the ability of ECs to produce NO and express eNOS gene, respectively. Although the downregulating effect of CRP was partially diminished by G-CSF, the negative effect of CRP was too dominant compared to the upregulating effects of G-CSF on NO production. And the effects of CRP and G-CSF on the secretion of the inflammatory cytokine interleukin-6 (IL-6) and endothelium-derived vasoactive factor endothelin-1 (ET-1) showed similar pattern. Conclusions: G-CSF itself augmented endothelial functions and CRP itself aggravated endothelial dysfunction. In combination the negative effects of CRP on endothelial function were too dominant for G-CSF. So the degree of G-CSF mediated endothelial dysfunction might give rise and be correlated with the degree of G-CSF induced CRP production not with G-CSF itself.