Actin is associated with tissue injury in trauma patients and produces a hypercoagulable profile in vitro.

ABSTRACT:

Background

While tissue injury provokes fibrinolysis shutdown in trauma, the mechanism remains elusive. Cellular death causes release of structural proteins, including actin and myosin, which may interact with clot formation and structure. We hypothesized that tissue injury is associated with high circulating actin and that actin produces a hypercoagulable profile with decreased fibrinolysis in vitro.

Methods

Blood was collected from trauma activation patients at a single Level I trauma center for thrombelastography and proteomics. Proteomic analyses were performed through targeted liquid chromatography coupled with mass spectrometry using isotope-labeled standards for quantification of actin and its endogenous inhibitor gelsolin. Based on the results, we added physiologic c

SUBMITTER: Coleman JR 

PROVIDER: S-EPMC8610777 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature