Aim To study the injury effect of lipoprotein （a） ［Lp（a）］ on biological function of mouse bone marrow-derived endothelial progenitor cells （EPC）. Methods EPC were divided into control groups and five treatment groups with different concentrations （1, 10, 100, 300 and 600 mg/L） of Lp（a）. EPC were isolated by adherence culture and identified by binding of UEA-1, and uptake of acetylated low density lipoprotein （ac-LDL）. The abilities of survival, migration and adherence were detected by the MTT, Transwell and gelatin adherence assays respectively. The total length of the tube structures in each photograph was measured using Adobe Photoshop software 7.0. Results Lp（a） dose-dependently decreased the surival rate of EPC, 100 mg/L Lp（a） reduced it significantly and the maximum injury concentration was 300 mg/L. A significantly reduced migratory rate of EPC could be seen after treatment with 1 mg/L Lp（a）, the count of the migratory cells was less than 1/6 of the control, so 1/9 for 10 mg/L Lp（a） and 1/14 for 300 mg/L Lp（a）. EPC treated with Lp（a） showed a dose-dependent decrease of adhesion to gelatin. 1 mg/L Lp（a） markedly decreased the number of adhesive cells （145.2±8.4/every field vs 115.2±12.6/ every field, P<0.05, n5）. When EPC were exposed to 10 or 100 mg/L Lp（a）, the capability of adhesion had further descended. When at 300 mg/L, it was remarkably descent to 1/16 of control. Treatment with 10 mg/L Lp（a） impaired the ability of EPC to form tube structures. EPC cultivanted with 100 mg/L had presented decreased tube formation and was less than 1/4 of control （36.34±1.54 mm/field vs 8.76±0.62 mm/field, P<0.001, n5）, and when incubated at 300 mg/L of Lp（a）, the integrity tube structure was severely disrupted. After treated with 100 mg/L of Lp（a）, not only the EPC colony-forming was decreased （10.2±1.3 vs 3.1±0.4, P<0.01, n5） but also the growth of the colony-forming was inhibited. Conclusions Lp（a） inhibited proliferation, migration, adhesion, vasogenesis, colony-forming capacity of EPC in a dose-dependent manner.