title: Microparticles in angiogenesis: therapeutic potential.
abstract: Considered during the past decades as cell dust, microparticles are now deemed true biomarkers and vectors of biological information between cells. Depending on their origin, the composition of microparticles varies and the subsequent message transported by them, such as proteins, mRNA, or miRNA, can differ. Recent studies have described microparticles as "cargos" of deleterious information in blood vessel wall under pathological situations such as hypertension, myocardial infarction, and metabolic syndrome. In addition, it has been reported that depending on their origin, microparticles also possess a therapeutic potential regarding angiogenesis. Microparticles can act directly through the interaction ligand/receptor or indirectly on angiogenesis by modulating soluble factor production involved in endothelial cell differentiation, proliferation, migration, and adhesion; by reprogramming endothelial mature cells; and by inducing changes in levels, phenotype, and function of endothelial progenitor cells. This results in an increase in formation of in vitro capillary-like tubes and the generation of new vessels in vivo under ischemic conditions, for instance. Taking into consideration these properties of microparticles, recent evidence provides new basis to expand the possibility that microparticles might be used as therapeutic tools in pathologies associated with an alteration of angiogenesis.
authors.affiliation: INSERM U694, Mitochondrie Régulations et Pathologie, Université d'Angers, Rue des Capucins, F-49100, Angers, France. carmen.martinez@univ-angers.fr
authors.forename: M Carmen
authors.initials: MC
authors.lastname: Martinez
authors.forename: Ramaroson
authors.initials: R
authors.lastname: Andriantsitohaina
mesh_terms: D000818:Animals; D055252:Cell-Derived Microparticles / Q000502:physiology*; D042783:Endothelial Cells / Q000166:cytology / Q000502:physiology; D055354:Exosomes / Q000502:physiology; D006801:Humans; D008659:Metabolic Diseases / Q000503:physiopathology; D009369:Neoplasms / Q000098:blood supply; D009389:Neovascularization, Pathologic / Q000209:etiology; D018919:Neovascularization, Physiologic / Q000502:physiology*; D013234:Stem Cells / Q000502:physiology