Table 1.

Endothelial injury methods and outcomes. (HUVEC, human umbilical vein endothelial cells; PSGL-1, P-selectin glycoprotein ligand-1; Par4, protease-activated receptor 4; TNF-α, tumour necrosis factor alpha; IFN-γ, interferon gamma; CCL2, C-C motif chemokine ligand 2; IL-1β, interleukin-1 beta; ApoE, apolipoprotein E; TF, tissue factor.)

vessel or cell type	injury method	key observations	references
cremaster arteriole	laser activation	laser activated endothelial cells trigger thrombus formation; neutrophil slow rolling on thrombus mediated by P-selectin-PSGL-1	[49]
cremaster arteriole and HUVEC	laser activation	endothelial activation precedes platelet accumulation; normal fibrin formation observed in Par4-/- mice	[50]
cremaster arteriole	laser activation	prothrombinase found on activated endothelial cells	[51]
cremaster arteriole	laser activation	neutrophils contain and express tissue factor at the site of laser injury; neutrophils accumulated before platelets	[52]
venule	TNF-α	TNF-α activated endothelial cells recruit neutrophils; platelets bind adherent neutrophils rather than endothelium	[49]
artery and HUVEC	TNF-α and IFN-γ	fractalkine causes degranulation, activation, and expression of platelet P-selectin on adherent platelets, mediating neutrophil recruitment	[53]
HUVEC	TNF-α	endothelial TF drives fibrin deposition and coagulation; upregulated ICAM can be targeted for delivering recombinant thrombomodulin to inflamed cells	[47]
cremaster arteriole	CCL2, TNF-α, IL-1β, or IFN-γ	platelets guide neutrophils to extravasation points via P-selectin-PSGL-1 and CD40/CD40 L	[54]
artery and HUVEC	ApoE-/- mice	increased endothelial stiffness causes enhanced leucocyte transendothelial migration	[55]
artery	ApoE-/- mice	reduced glycocalyx thickness and increased platelet adhesion occur at bifurcation point	[56]
artery	ApoE-/- mice	endothelial dysfunction and glycocalyx impairment coincide with endothelial-dependent vasodilation, permeability, and increases in atherosclerotic biomarkers	[4]