Εξειδίκευση τύπου :	Άρθρο σε επιστημονικό περιοδικό
Τίτλος:	Augmented oxidative stress, accumulation of DNA damage and impaired DNA repair mechanisms in thrombotic primary antiphospholipid syndrome
Δημιουργός/Συγγραφέας:	Pappa, Maria Ntouros, Panagiotis A Papanikolaou, Christina Sfikakis, Petros P [EL] Σουλιώτης, Βασίλης Λ.[EN] Souliotis, Vassilis L. Tektonidou, Maria G
Εκδότης:	Clinical Immunology
Ημερομηνία:	2023-07-16
Γλώσσα:	Αγγλικά
ISSN:	15216616
DOI:	10.1016/j.clim.2023.109693
Άλλο:	37454866
Περίληψη:	Antiphospholipid syndrome (APS) is a rare autoimmune disorder with complex pathogenesis. Studies have shown that oxidative stress may contribute to APS pathophysiology. In peripheral blood mononuclear cells (PBMCs) from thrombotic Primary APS (thrPAPS) patients and age/sex-matched healthy controls (HC), as well as a control group of asymptomatic antiphospholipid antibody (aPL) positive individuals without APS (aPL+/non-APS), we examined oxidative stress, abasic (apurinic/apyrimidinic) sites, and DNA damage response (DDR)-associated parameters, including endogenous DNA damage (single- and double-strand breaks) and DNA repair mechanisms, namely nucleotide excision repair (NER) and double-strand breaks repair (DSB/R). We found that thrPAPS patients exhibited significantly higher levels of endogenous DNA damage, increased oxidative stress and abasic sites, as well as lower NER and DSB/R capacities versus HC (all P < 0.001) and versus aPL+/non-APS subjects (all P < 0.05). Our findings demonstrate that oxidative stress and decreased DNA repair mechanisms contribute to the accumulation of endogenous DNA damage in PBMCs from thrPAPS patients and, if further validated, may be exploited as therapeutic targets and potential biomarkers.
Τίτλος πηγής δημοσίευσης:	Clinical immunology (Orlando, Fla.)
Τόμος/Κεφάλαιο:	254
Θεματική Κατηγορία:	[EL] Ιατρική[EN] Medicine [EL] Ανοσολογία[EN] Immunology [EL] Βιοχημεία[EN] Biochemistry
Λέξεις-Κλειδιά:	DNA damage response Double-strand breaks repair Endogenous DNA damage Nucleotide excision repair Oxidative stress Primary antiphospholipid syndrome Humans Leukocytes, Mononuclear DNA Repair Oxidative Stress DNA Damage Antiphospholipid Syndrome Thrombosis
Ηλεκτρονική διεύθυνση στον εκδότη (link):	https://www.sciencedirect.com/science/article/pii/S1521661623004564?via%3Dihub
Εμφανίζεται στις συλλογές:	Ινστιτούτο Χημικής Βιολογίας - Επιστημονικό έργο