TNFα-Damaged-HUVECs Microparticles Modify Endothelial Progenitor Cell Functional Activity

Endothelial progenitor cells (EPCs) have an important role in the maintenance of vascular integrity and homeostasis. While there are many studies that explain EPCs mechanisms action, there are few studies that demonstrate how they interact with other emerging physiological elements such as Endotheli...

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Detalles Bibliográficos
Autores: Luna, Carlos, Carmona, Andrés, Alique, Matilde, Carracedo Añón, Julia María, Ramírez, Rafael
Tipo de recurso: artículo
Fecha de publicación:2015
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/131422
Acceso en línea:https://hdl.handle.net/20.500.14352/131422
Access Level:acceso abierto
Palabra clave:612.1
616.1
616.15
576
Endothelial microparticles
Endothelial progenitor cells
Angiogenesis
TNFalpha
HUVECs
Fisiología
Sistema cardiovascular
Hematología
Biología celular (Biología)
2411.03 Fisiología Cardiovascular
3207.04 Patología Cardiovascular
3207.08 Hematología
2410.03 Citología Humana
Descripción
Sumario:Endothelial progenitor cells (EPCs) have an important role in the maintenance of vascular integrity and homeostasis. While there are many studies that explain EPCs mechanisms action, there are few studies that demonstrate how they interact with other emerging physiological elements such as Endothelial Microparticles (EMPs). EMPs are membranous structures with a size between 100 and 1000 nm that act as molecular information transporter in biological systems and are known as an important elements in develop different pathologies; moreover a lot of works explains that are novel biomarkers. To elucidate these interactions, we proposed an in vitro model of endothelial damage mediated by TNFalpha, in which damaged EMPs and EPCs are in contact to assess EPCs functional effects. We have observed that damaged EMPs can modulate several EPCs classic factors as colony forming units (CFUs), contribution to repair a physically damaged endothelium (wound healing), binding to mature endothelium, and co-adjuvants to the formation of new vessels in vitro (angiogenesis). All of these in a dose-dependent manner. Damaged EMPs at a concentration of 103 MPs/ml have an activating effect of these capabilities, while at concentrations of 105 MPs/ml these effects are attenuated or reduced. This in vitro model helps explain that in diseases where there is an imbalance between these two elements (EPCs and damaged EMPs), the key cellular elements in the regeneration and maintenance of vascular homeostasis (EPCs) are not fully functional, and could explain, at least in part, endothelial dysfunction associated in various pathologies.