2026-08-05T15:43:16Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/83362024-11-29T19:27:11Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Borghesan, Michela author Fafián-Labora, Juan author Eleftheriadou, Olga author Carpintero-Fernández, Paula author Paez-Ribes, Marta author Vizcay-Barrena, Gema author Swisa, Avital author Kolodkin-Gal, Dror author Ximénez-Embún, Pilar author Lowe, Robert author Martín-Martín, Belen author Peinado Selgas, Hector author Muoz Peralta, Javier author Fleck, Roland A author Dor, Yuval author Ben-Porath, Ittai author Vossenkamper, Anna author Muñoz-Espin, Daniel author O'Loghlen, Ana author 2019-06-25 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. Cell Rep. 2019;27(13):3956-3971. 10.1016/j.celrep.2019.05.095 2211-1247 22111247 Cell reports 31242426 http://hdl.handle.net/20.500.12105/8336 DDIS EV IFITM3 OIS Aging Exosomes Fragilis Interferon Paracrine senescence Small extracellular vesicles Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3