Alternative Complement Pathway Activation Provokes a Hypercoagulable State with Diminished Fibrinolysis.

ABSTRACT:

Introduction

Several disease processes trigger prolonged activation of the alternative complement pathway. Crosslinks between complement activation and physiologic changes in platelets and neutrophils have been identified, but how this interplay alters the hemostatic potential in humans remains undefined. We hypothesize that activation of the alternative pathway triggers a hypercoagulable state.

Methods

C3/C5 convertase Cobra Venom Factor (CVF, 10 Units/mL) was employed to activate the alternative complement pathway in whole blood. Complement inhibition was completed with inhibitors for C3/C3b (Compstatin, 25 and 50 μM), C3a receptor (SB290157, 300 nM, C3aR), and C5a receptor (W54011, 6 nM, C5aR). Coagulation was assessed using native thrombelastography which produces the fo

SUBMITTER: Samuels JM 

PROVIDER: S-EPMC7033000 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature