Thrombosis research · 2005
Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines.
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Olwill Shane A, McGlynn Hugh, Gilmore William S, Alexander H Denis
Аннотация
INTRODUCTION: Acute promyelocytic leukaemia (APL) (M3) is associated with both a characteristic t(15;17) and severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis. It has been suggested that annexin II, a coreceptor for tissue plasminogen activator (t-PA) and plasminogen (PLG), is overexpressed on the surface of promyelocytes, leading to an increased fibrinolytic potential.
MATERIALS AND METHODS: This study examined the level of annexin II cell surface and mRNA expression in a range of acute myeloid leukaemia (AML) cell lines. The evidence that annexin II levels are higher in APL would lend support to the hypothesis that the bleeding disorder seen in APL is caused by hyperfibrinolysis.
RESULTS: Cell surface annexin II was found to be expressed at higher levels on NB4 (promyelocytic) cells than on either KG1a (early myeloid) or HL60 (myelocytic) cells. However, even higher levels were found on U937 and MM6 (histo-monocytic) and HEL (erythroid) cells (p<0.01). MM6 cells showed a threefold increase in annexin II mRNA compared to any of the other cell lines.
CONCLUSIONS: These findings do not fully support the concept of the coagulopathy associated with APL being caused by hyperfibrinolysis alone. Further investigations are required to identify the significance of annexin II expression and regulation in leukaemia.
MATERIALS AND METHODS: This study examined the level of annexin II cell surface and mRNA expression in a range of acute myeloid leukaemia (AML) cell lines. The evidence that annexin II levels are higher in APL would lend support to the hypothesis that the bleeding disorder seen in APL is caused by hyperfibrinolysis.
RESULTS: Cell surface annexin II was found to be expressed at higher levels on NB4 (promyelocytic) cells than on either KG1a (early myeloid) or HL60 (myelocytic) cells. However, even higher levels were found on U937 and MM6 (histo-monocytic) and HEL (erythroid) cells (p<0.01). MM6 cells showed a threefold increase in annexin II mRNA compared to any of the other cell lines.
CONCLUSIONS: These findings do not fully support the concept of the coagulopathy associated with APL being caused by hyperfibrinolysis alone. Further investigations are required to identify the significance of annexin II expression and regulation in leukaemia.