Table 2.

MPs as mediators of communication between cells.

Effects	Cell source of MPs → target cell	In vitro generation of MPs	Content of MPs	REF
Chemotaxis of mononuclear phagocytes to the endothelium	Platelets → endothelial cells	Apoptosis	RANTES/CCL5	[54]
Nonspecific chemotaxis	Platelets → human neutrophils	PGE1	Fibrinogen receptor Glycoproteins and integrin αIIbβ3	[33, 55]
Effects on cell proliferation and differentiation	Platelets → endothelial cells Tumoral cells (human)	Cells activation and starvation	miRNA	[56, 57]
	Platelets → endothelial precursors Tumoral cells → different types of cells	PGE1	Epidermal growth factor receptor	[33, 55]
Apoptosis of endothelial cells and inhibition of osteoclastogenesis in RA	Platelets → endothelial cells, osteoclast	Activation	miRNA-223	[58]
Induction of GLUT4 expression in insulin-resistant cells	Platelets → endothelial cells	Activation	miRNA-223	[59, 60]
Endothelial activation	Myeloid pyroptotic and activated cells → endothelium and leukocytes (humans)	Apoptosis	IL-1-β	[54]
Synthesis of sphingomyelinase, M2 activation, and cell death	Human macrophages → endothelial cells	Calcium-mediated apoptosis	AA	[61, 62]
Coagulation, cell transformation, and inhibition of endothelial cells	Mononuclear, endothelial, and tumoral cells → platelets	Staurosporine-induced apoptosis	Cardiolipin, platelet activating factor	[63, 64]
Coagulation	Mononuclear cells → platelets, megakaryocytes	Apoptosis	CCR5	[65]
	Monocytes → platelets (humans)	Thrombin activation	Tissue factor	[33, 55]
Antigen presentation, cross-presentation, and anergy	Among leukocytes (humans)	Apoptosis	MHC	[33, 55]
Expression of receptors from other cellular origins and transformation	Tumor, stem, and endothelial precursor cells → platelets, myeloid cell lines (humans)	Overgrowth and activation	mRNA	[66–68]