Do extracellular histones increase plasma thrombin generation by impairing thrombomodulin-dependent protein C activation?
Histones enhance plasma thrombin generation by reducing TM-dependent protein C activation. This mechanism might contribute to microvascular thrombosis induced by histones in vivo at sites of organ failure or severe inflammation.
Adoptive transfer of Tregs dose-dependently changed plaque composition to a stable plaque phenotype and lowered the incidence of plaque disruption in ApoE-/- mice. The major mechanisms involved reduced expression of inflammatory cytokines and MMP-2 and MMP-9, and enhanced expression of P4Hα1 in the carotid plaque. Tregs may provide a novel approach to the treatment of vulnerable plaques.