Objective      To determine the effects of stanniocalcin 1 (STC1) on the proliferation and migration of endothelial progenitor cells (EPCs)

and investigate the potential mechanism involved.       Methods      EPCs were isolated from the spleens of Sprague-Dawley rats by density-gradient centrifugation

and then cultured and identified with double-fluorescent immunostaining. These EPCs were treated with recombinant human STC1 at different concentrations

or transfected with its siRNA to silence the STC1 expression. The proliferation and migration properties of these EPCs as well as the effects of STC1 on the expression levels of protein kinase B (Akt)

endothelial nitric oxide synthase (eNOS) and their phosphorylation were detected. Selective phosphatidyl inositol 3 kinase (PI3K) inhibitor (LY294002) and eNOS inhibitor (L-NAME) were used to reverse the response of pre-treated EPCs to rhSTC1.       Results      Double-fluorescent immunostaining indicated that the purity of our EPCs was about 88.5%. Exogenous rhSTC1 treatment promoted the proliferation and migration of EPCs in a dose-dependent manner via the PI3K/Akt/eNOS pathway activation

which was reflected by the increasing of Akt and eNOS phosphorylation levels. Endogenous STC1-expression silence interfered the proliferation and migration of EPCs

and inhibitors LY294002 and L-NAME inhibited the rhSTC1-induced effect on pre-treated EPCs by blocking PI3K/Akt/eNOS pathway.       Conclusion      STC1 enhances EPCs to proliferate and migrate by activating PI3K/Akt/eNOS pathway. Our findings maybe provide a new therapeutic target for the repair of injured vascular endothelium.