In order to study the role of annexin Ⅱ, a recombinant expression vector, pZeoSV2(+)ANN Ⅱ, containing the annexin Ⅱ cDNA , was developed. The 1.1 kb length annexin Ⅱ cDNA was inserted into a express ion vector, PZeoSV(+) and transfected into HL 60 cells which had low baseline e xpression of Ann Ⅱ. pZeoSV(+) ANNⅡ was analyzed by restriction mapping and th e Ann Ⅱ sequence identified. The ability of the transfected cells, non transf ected and mock transfected cells to stimulate t PA depend plasminogen activat ion was compared. The results showed that HL 60 with pZeoSV(+)ANNⅡ transfectio n could significantly increase the plasminogen activation (8.9±1.2 U) in vitr o with the difference being significant as compared with non transfected (1.5±0. 4 U) and mock transfected cells (4.2±0.9 U), respectively. AntiannexinⅡoligon ucleotides significantly inhibited the binding ability of t PA and plasminogen to annexinⅡ, and obviously reduced the plasminogen activation in vitro . The above findings showed human umbilical vein endothelial cells (HUVECs) treated w ith sense or missense oligonucleotides indicated no significant change in bindin g of t PA and PLG. Treatment of HUVECs with antiannexin Ⅱ oligonucleotides cou ld significantly reduce the plasminogen activation by 2.4±0.3 U as compared wit h sense oligonucleotide group in binding of t PA and PLG. These results, theref ore, suggest that Ann Ⅱ can bind plasminogen and participate in the stimulatio n of t PA dependent activation of plasminogen, and that interference with Ann Ⅱ mRNA by antisense oligonucleotide may be a new strategy for the therapy of bleeding in patients with hyperfibrinolysis. In order to study the role of annexin II, a recombinant expression vector, pZeoSV2 (+) ANN II, containing the annexin II cDNA, was developed. The 1.1 kb length annexin II cDNA was inserted into a express ion vector, PZeoSV and transfected into HL 60 cells which had low baseline e xpression of Ann II. pZeoSV (+) ANN II was analyzed by restriction mapping and th e Ann II sequence identified. The ability of the transfected cells, non transf ected and mock transfected cells to stimulate The results showed that HL60 with pZeoSV (+) ANNII transfectio n could significantly increase the plasminogen activation (8.9 ± 1.2 U) in vitr o with the difference being significant as compared with non transfected (1.5 ± 0.4 U) and mock transfected cells (4.2 ± 0.9 U), respectively. Antiannexin Ⅱ ligon ucleotides significantly inhibited the binding ability of t PA and plasminogen to annexin II, and significantly reduced the plasminoge n activation in vitro. The above findings showed human umbilical vein endothelial cells (HUVECs) treated w ith sense or missense oligonucleotides indicated no significant change in bindin g of t PA and PLG. Treatment of HUVECs with antiannexin II oligonucleotides cou ld significantly reduce the plasminogen activation by 2.4 ± 0.3 U as compared wit h sense oligonucleotide group in binding of t PA and PLG. These results, there ore, suggest that Ann II can bind plasminogen and participate in the stimulant n of t PA dependent activation of plasminogen, and that interference with Ann II mRNA by antisense oligonucleotide may be a new strategy for the therapy of bleeding in patients with hyperfibrinolysis.