Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein IFITM3
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Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein IFITM3Author(s)
Date
2019-06-25Citation
Borghesan M, Fafián-Labora J, Eleftheriadou O, Carpintero-Fernández P, Paez-Ribes M, Vizcay-Barrena G, Swisa A, Kolodkin-Gal D, Ximénez-Embún P, Lowe R, Martín-Martín B, Peinado H, Muñoz J, Fleck RA, Dor Y, Ben-Porath I, Vossenkamper A, Muñoz-Espin D, O'Loghlen A. Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein IFITM3. Cell Rep. 2019 Jun 25;27(13):3956-3971.e6.
Abstract
[Abstract] 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.
Keywords
DDIS
EV
IFITM3
OIS
Aging
Exosomes
Fragilis
Interferon
Paracrine senescence
Small Extracellular vesicles
EV
IFITM3
OIS
Aging
Exosomes
Fragilis
Interferon
Paracrine senescence
Small Extracellular vesicles
Editor version
Rights
Creative Commons Attribution 4.0 International License (CC-BY 4.0)
ISSN
2211-1247