Figure 4.
Figure 4. Purified hnDNA enhances low-concentration TF–initiated TG by amplifying thrombin-dependent FXI activation. Amplification effect of hnDNA on TG triggered by 1 pM TF in PFP (A) or in FXII-deficient plasma (Def-XII; 25 μg/mL hnDNA) (B) or in FXI-deficient plasma (Def-XI; 25 μg/mL hnDNA) (C). (D) Comparison of peak TG (mean + standard deviation) in the presence or absence of 25 μg/mL hnDNA in FXII- or FXI-deficient plasma. (E) Amplification effect of 50 μg/mL hnDNA on FXIa generation following 10 nM α-thrombin (IIa)–dependent activation of 30 nM FXI in the presence of physiologic concentration of HMWK in buffer. (F) Absence of an amplification effect of intact NETs on 1 pM TF-initiated TG in PFP. A23187, ionophore (5 μM); PMN, human neutrophils. PMA (600 nM). Panels A-C and F are representative of independent experiments performed at least 3 times. Mean values for 3 independent experiments in panels C and D.

Purified hnDNA enhances low-concentration TF–initiated TG by amplifying thrombin-dependent FXI activation. Amplification effect of hnDNA on TG triggered by 1 pM TF in PFP (A) or in FXII-deficient plasma (Def-XII; 25 μg/mL hnDNA) (B) or in FXI-deficient plasma (Def-XI; 25 μg/mL hnDNA) (C). (D) Comparison of peak TG (mean + standard deviation) in the presence or absence of 25 μg/mL hnDNA in FXII- or FXI-deficient plasma. (E) Amplification effect of 50 μg/mL hnDNA on FXIa generation following 10 nM α-thrombin (IIa)–dependent activation of 30 nM FXI in the presence of physiologic concentration of HMWK in buffer. (F) Absence of an amplification effect of intact NETs on 1 pM TF-initiated TG in PFP. A23187, ionophore (5 μM); PMN, human neutrophils. PMA (600 nM). Panels A-C and F are representative of independent experiments performed at least 3 times. Mean values for 3 independent experiments in panels C and D.

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