Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/8336
Título
Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3
Autor(es)
Borghesan, Michela | Fafián-Labora, Juan | Eleftheriadou, Olga | Carpintero-Fernández, Paula | Paez-Ribes, Marta | Vizcay-Barrena, Gema | Swisa, Avital | Kolodkin-Gal, Dror | Ximénez-Embún, Pilar | Lowe, Robert | Martín-Martín, Belen | Peinado Selgas, Hector CNIO | Muoz Peralta, Javier CNIO | Fleck, Roland A | Dor, Yuval | Ben-Porath, Ittai | Vossenkamper, Anna | Muñoz-Espin, Daniel | O'Loghlen, Ana
Fecha de publicación
2019-06-25
Cita
Cell Rep. 2019;27(13):3956-3971.
Idioma
Inglés
Tipo de documento
journal article
Resumen
Senescence is a cellular phenotype present in health and disease, characterized by a stable cell-cycle arrest and an inflammatory response called senescence-associated secretory phenotype (SASP). The SASP is important in influencing the behavior of neighboring cells and altering the microenvironment; yet, this role has been mainly attributed to soluble factors. Here, we show that both the soluble factors and small extracellular vesicles (sEVs) are capable of transmitting paracrine senescence to nearby cells. Analysis of individual cells internalizing sEVs, using a Cre-reporter system, show a positive correlation between sEV uptake and senescence activation. We find an increase in the number of multivesicular bodies during senescence in vivo. sEV protein characterization by mass spectrometry (MS) followed by a functional siRNA screen identify interferon-induced transmembrane protein 3 (IFITM3) as being partially responsible for transmitting senescence to normal cells. We find that sEVs contribute to paracrine senescence.
Palabras clave
DDIS | EV | IFITM3 | OIS | Aging | Exosomes | Fragilis | Interferon | Paracrine senescence | Small extracellular vesicles
Versión en línea
DOI
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