Figure 4.
3E8 anti-HK antibody has the same effects on Aβ42-induced FXII activation as does the absence of HK in human plasma. NHP or KN-DF human plasma was incubated with buffer, 3E8 (0.5 μM), or control IgG (0.5 μM) at 37°C for 20 minutes. Then Aβ42 (5 μM) was added and incubated at 37°C for 2 hours. Western blotting analyses were performed with antibodies against FXII/FXIIa, HK, and TF. In the absence of 3E8, Aβ42 induced FXII activation and HK cleavage in normal plasma (lane 2 in [A-B]). It also induced a small but significant activation of FXII in KN-DF human plasma (lane 6 in [A-B]). 3E8 blocked FXII activation in normal plasma but had no significant effect on FXII activation in KN-DF plasma (lane 7 in [A-B]). Control IgG did not affect Aβ42-induced FXII or HK changes. FXIIa and HK signals were normalized to TF. n = 6. Data are denoted as mean ± SEM. *P < .05, ***P ≤ .001. P > .05 was not significant (n.s.).

3E8 anti-HK antibody has the same effects on Aβ42-induced FXII activation as does the absence of HK in human plasma. NHP or KN-DF human plasma was incubated with buffer, 3E8 (0.5 μM), or control IgG (0.5 μM) at 37°C for 20 minutes. Then Aβ42 (5 μM) was added and incubated at 37°C for 2 hours. Western blotting analyses were performed with antibodies against FXII/FXIIa, HK, and TF. In the absence of 3E8, Aβ42 induced FXII activation and HK cleavage in normal plasma (lane 2 in [A-B]). It also induced a small but significant activation of FXII in KN-DF human plasma (lane 6 in [A-B]). 3E8 blocked FXII activation in normal plasma but had no significant effect on FXII activation in KN-DF plasma (lane 7 in [A-B]). Control IgG did not affect Aβ42-induced FXII or HK changes. FXIIa and HK signals were normalized to TF. n = 6. Data are denoted as mean ± SEM. *P < .05, ***P ≤ .001. P > .05 was not significant (n.s.).

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