Exosomes as Radiation Biomarkers

Extracellular Vesicles

Jella, Kishore Kumar. 2022. “Exosomes as Radiation Biomarkers.” NATO Science for Peace and Security Series A: Chemistry and Biology, 125–36. https://doi.org/10.1007/978-94-024-2101-9_8.

Exosomes are now considered as important mediators of intercellular communication. The exosome cargo contains proteins; mRNA, microRNA (miRNA) and DNA that delivers the information between one cell to other cells can play an important role in identifying the pathophysiological conditions of any cell. Increased understanding of mechanism about exosome release and its communication could provide a novel strategy for the development of biomarkers in various health conditions. Recent shreds of evidence revealed that radiation induces the secretion and alters the composition of exosomes released from radiated cells. The exosomes released from radiated cells alters the signaling pathways in recipient cells. Unraveling the mechanisms related to radiation and exosomes would shed light on the unknown factors that are involved in radiation-induced non-targeted effects. This can provide pavement for the development of biomarkers in radiation emergency situations.

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Cigarette smoke (CS) represents one of the most relevant environmental risk factors for several chronic pathologies. Tissue damage caused by CS exposure is mediated, at least in part, by oxidative stress induced by its toxic and pro-oxidant components. Evidence demonstrates that extracellular vesicles (EVs) released by various cell types exposed to CS extract (CSE) are characterized by altered biochemical cargo and gained pathological properties. In the present study, we evaluated the content of oxidized proteins and phospholipid fatty acid profiles of EVs released by human bronchial epithelial BEAS-2B cells treated with CSE. This specific molecular characterization has hitherto not been performed. After confirmation that CSE reduces viability of BEAS-2B cells and elevates intracellular ROS levels, in a dose-dependent manner, we demonstrated that 24 h exposure at 1% CSE, a concentration that only slight modifies cell viability but increases ROS levels, was able to increase carbonylated protein levels in cells and released EVs. The release of oxidatively modified proteins via EVs might represent a mechanism used by cells to remove toxic proteins in order to avoid their intracellular overloading. Moreover, 1% CSE induced only few changes in the fatty acid asset in BEAS-2B cell membrane phospholipids, whereas several rearrangements were observed in EVs released by CSE-treated cells. The impact of changes in acyl chain composition of CSE-EVs accounted for the increased saturation levels of phospholipids, a membrane parameter that might influence EV stability, uptake and, at least in part, EV-mediated biological effects. The present in vitro study adds new information concerning the biochemical composition of CSE-related EVs, useful to predict their biological effects on target cells. Furthermore, the information regarding the presence of oxidized proteins and the specific membrane features of CSE-related EVs can be useful to define the utilization of circulating EVs as marker for diagnosing of CS-induced lung damage and/or CS-related diseases.

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