Abstract 161 Extracellular vesicles derived from patients with atrial fibrillation and coronary heart disease promote inflammation and apoptosis in human endothelial cells

Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02302-4
Extracellular vesicles derived from patients with atrial fibrillation and coronary heart disease promote inflammation and apoptosis in human endothelial cells
M. Tangos¹, V. Nageswaran², P. Ramezani Rad², A. Haghikia², M. Lodi³, F. Heringhaus⁴, K. Jaquet⁵, C. Hanefeld⁶, A. Mügge⁴, N. Hamdani⁷, für die Studiengruppe: AG13
¹Abteilung für Zelluläre und Translationale Physiologie, Ruhr-Universität Bochum, Bochum; ²CC 11: Med. Klinik für Kardiologie, Charité - Universitätsmedizin Berlin, Berlin; ³Neuroanatomie und Molekulare Hirnforschung, Ruhr-Universität Bochum, Bochum; ⁴Medizinische Klinik II, Kardiologie, Klinikum der Ruhr-Universität Bochum, Bochum; ⁵Molekulare Kardiologie, Ruhr-Universität Bochum, Bochum; ⁶Medizinische Klinik, St. Elisabeth-Hospital GmbH, Bochum; ⁷Cellular Physiology, Kath. Klinikum Bochum, Bochum;
Cardiovascular diseases (CVD) and two of its manifestations, atrial fibrillation (AF) and coronary heart disease (CHD), put a massive burden on patient’s health and significantly decrease the quality of life. Here we studied the pivotal role of extracellular vesicles (EVs) in promoting pathophysiological changes in CVD, as they participate in the transport of bioactive molecules throughout the blood stream. We utilized transmission electron microscopy (TEM) and western blot to verify successful EVs isolation from 1 ml blood plasma. RNA content of EVs isolated from patients was sequenced to identify up- or downregulated RNAs. Using human aortic endothelial cells (HAECs), we investigated if EVs isolated from patients trigger inflammation- and apoptosis-related events and we performed stress assays. We found several long non-coding RNAs to be significantly downregulated in EVs isolated from CVD patients targeting genes associated with the process of inflammation, apoptosis, oxidative stress and respiration. These results coincide with our findings that EVs isolated from CVD patients were able to trigger inflammation and apoptosis in HAECs. In addition, EVs isolated from AF patients negatively affected mitochondrial function of HAECs. Our results emphasize the role of EV in disease development and highlight potential targets for treatment. Overall, we believe that the dynamics of EV-derived lncRNAs and gene interactions represent an important mediator of pathophysiological alterations and should be investigated in the future. However, the lack of standardized EV isolation protocols, great variety of content, use of different EV sources, and subpopulations massively impede vesicle research and underline the need for further data collection.
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