Circulating Endothelial Microparticles: A Key Hallmark of Atherosclerosis Progression

Table 2

Scientific work on microparticle in association with its link with atherosclerosis.

Microparticles	Role in atherosclerosis	Reference
PMPs	Enhance cyclooxygenase-2 (COX-2) and intracellular adhesion molecules-1 (ICAM-1) release.	[28]
	COX-2 expression in monocytes through translocation of protein kinase C (PKC) from cytosol to the cell membrane.	[29]
	Enhance the adhesion of monocyte to human umbilical vein endothelial cells.	[30]
	Increase WBC aggregation and assembly via expression of P-selectin.	[31]
	Neutrophil aggregation and enhance phagocytic activity.	[32]
EMPs	CD-144/vascular endothelial cadherin positive.	[33]
	Reactive oxygen spices (ROS) formation.	[34]
	Matrix metalloproteinase-2 (MMP-2) activation and vascular matrix remodeling.	[35, 36]
	Reduce expression of p38-MAPK in human aortic endothelial cells caused reduction of TNF- induced EMPs.	[37]
	EMPs exhibit the TF activity in atherosclerotic plaques.	[38]
	Expression of E-selectin, ICAM-1, and VCAM-1.	[39]
MMPs	Inducible nitric oxide synthase (iNOS) activation.	[40]
	Extracellular signal-regulated kinases (ERK1/2) activation.	[41]
	Procoagulant substances responsible for endothelial dysfunction.	[25]
	IL-1β in MMPs can enhance the vascular inflammatory.	[42]
	Atherosclerotic plaque formation in the ApoE mice.	[27]
	Increased expression of apoptosis regulator Bax, caspase-8, caspase-3, and cytochrome C in cardiomyocytes.	[43]
	Induce superoxide anion production, inflammatory cytokine release, and activation of NF-B gene in monocytes.	[44]