Characterization of plasma-derived small extracellular vesicles indicates ongoing endothelial and platelet activation in patients with thrombotic antiphospholipid syndrome

Štok, Ula (avtor), Blokar, Elizabeta (avtor), Lenassi, Metka (avtor), Holcar, Marija (avtor), Frank Bertoncelj, Mojca (avtor), Erman, Andreja (avtor), Resnik, Nataša (avtor), Sodin-Šemrl, Snežna (avtor), Čučnik, Saša (avtor), Perdan-Pirkmajer, Katja (avtor), Ambrožič, Aleš (avtor), Žigon, Polona (avtor)

Antiphospholipid syndrome (APS) is a systemic autoimmune disease, characterized by thrombosis, obstetric complications and the presence of antiphospholipid antibodies (aPL), which drive endothelial injury and thrombophilia. Extracellular vesicles (EVs) have been implicated in endothelial and thrombotic pathologies. Here, we characterized the quantity, cellular origin and the surface expression of biologically active molecules in small EVs (sEVs) isolated from the plasma of thrombotic APS patients (n = 14), aPL-negative patients with idiopathic thrombosis (aPL-neg IT, n = 5) and healthy blood donors (HBD, n = 7). Nanoparticle tracking analysis showed similar sEV sizes (110–170 nm) between the groups, with an increased quantity of sEVs in patients with APS and aPLneg IT compared to HBD. MACSPlex analysis of 37 different sEV surface markers showed endothelial (CD31), platelet (CD41b and CD42a), leukocyte (CD45), CD8 lymphocyte and APC (HLA-ABC) cell-derived sEVs. Except for CD8, these molecules were comparably expressed in all study groups. sEVs from APS patients were specifically enriched in surface expression of CD62P, suggesting endothelial and platelet activation in APS. Additionally, APS patients exhibited increased CD133/1 expression compared to aPL-neg IT, suggesting endothelial damage in APS patients. These findings demonstrate enhanced shedding, and distinct biological properties of sEVs in thrombotic APS.

• Jezik: Angleški jezik
• Ključne besede: antiphospholipid syndrome, thrombosis, adhesion molecules, small extracellular vesicles, surface protein markers, endothelial activation, platelet activation
• Vrsta gradiva: Članek v reviji
• Tipologija: 1.01 - Izvirni znanstveni članek
• Organizacija: FFA - Fakulteta za farmacijo ; MF - Medicinska fakulteta
• Status publikacije: Objavljeno
• Različica publikacije: Objavljena publikacija
• Leto izida: 2020
• Št. strani: 13 str.
• Številčenje: Vol. 9, iss. 5, art. 1211
• PID: 20.500.12556/RUL-133736
• UDK: 616.1
• ISSN pri članku: 2073-4409
• DOI: 10.3390/cells9051211
• COBISS.SI-ID: 15921155
• Datum objave v RUL: 13.12.2021

Gradivo je del revije

• Naslov: Cells
• Skrajšan naslov: Cells
• Založnik: MDPI
• ISSN: 2073-4409
• COBISS.SI-ID: 519958809

Licence

• Licenca: CC BY 4.0, Creative Commons Priznanje avtorstva 4.0 Mednarodna
• Povezava: http://creativecommons.org/licenses/by/4.0/deed.sl
• Opis: To je standardna licenca Creative Commons, ki daje uporabnikom največ možnosti za nadaljnjo uporabo dela, pri čemer morajo navesti avtorja.
• Začetek licenciranja: 13.05.2020

Sekundarni jezik

• Jezik: Slovenski jezik
• Ključne besede: antifosfolipidni sindrom, tromboza, adhezijske molekule