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001-es BibID:BIBFORM116479
035-os BibID:(cikkazonosító)6829 (scopus)85176548280 (WoS)001099491300001
Első szerző:Illési Ádám (orvos)
Cím:Technically Challenging Percutaneous Interventions of Chronic Total Occlusions Are Associated with Enhanced Platelet Activation / Illési Ádám, Fejes Zsolt, Pócsi Marianna, Debreceni Ildikó Beke, Hodosi Katalin, Nagy Jr. Béla, Kappelmayer János, Kőszegi Zsolt, Csanádi Zoltán, Szük Tibor
Dátum:2023
ISSN:2077-0383
Megjegyzések:Percutaneous coronary intervention (PCI) is a frequently performed treatment option for recanalization in patients with chronic total occlusion (CTO). As CTO-PCIs are often complicated and challenging for interventionalists, the stressful and damaging nature of the procedure can be remarkable, thus platelets can be easily activated. Our aim was to investigate the effect of CTO-PCI on platelet activation and the expression of selected circulating microRNAs (miR) of platelet and endothelium origin after CTO-PCI. In this study, 50 subjects after CTO-PCI were enrolled. Blood samples were obtained before PCI, at 2 days and 3?6 months after the procedure to measure the degree of platelet activation and the level of plasma miR-223, miR-181b, and miR-126. Patients were divided based on the characteristics of the intervention. Patients with higher Japanese CTO scores and longer duration of PCI showed significantly elevated platelet P-selectin positivity (p = 0.004 and p = 0.013, respectively) 2 days after the procedure compared to pre-PCI and increased concentration of soluble P-selectin 3?6 months after the intervention (higher Japanese CTO score: p = 0.028 and longer duration of PCI: p = 0.023) compared to baseline values. Shorter total stent length caused a significantly lower miR-181b expression at 3?6 months after the intervention (p = 0.031), while no difference was observed in miR-223 and miR-126. One stent thrombosis occurred during the follow-up period. Although these technically challenging CTO-PCIs may cause enhanced platelet activation right after the intervention and long-term endothelial cell dysfunction, these interventions are not associated with more adverse clinical events.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
biomarker
chronic total coronary occlusion
coronary intervention
microRNA
platelet activation
Megjelenés:Journal of Clinical Medicine. - 12 : 21 (2023), p. 1-14. -
További szerzők:Fejes Zsolt (1988-) (molekuláris biológus) Pócsi Marianna (1989-) (klinikai laboratóriumi kutató) Bekéné Debreceni Ildikó (1970-) (biológus) Hódosi Katalin Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Kappelmayer János (1960-) (laboratóriumi szakorvos) Kőszegi Zsolt (1962-) (kardiológus, belgyógyász) Csanádi Zoltán (1960-) (kardiológus) Szűk Tibor (1967-) (kardiológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
ÚNKP-22-4-II-DE-120
Egyéb
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001-es BibID:BIBFORM121594
035-os BibID:(Scopus)85191442861
Első szerző:Krajcsir Bálint
Cím:Ponatinib Induces a Procoagulant Phenotype in Human Coronary Endothelial Cells via Inducing Apoptosis / Bálint Krajcsir, Marianna Pócsi, Zsolt Fejes, Béla Nagy Jr., János Kappelmayer, Ildikó Beke Debreceni
Dátum:2024
ISSN:1999-4923
Megjegyzések:BCR-ABL tyrosine kinase inhibitors (TKIs) are effective drugs in the treatment of patients with chronic myeloid leukemia. However, based on clinical studies, ponatinib was associated with the development of thrombotic complications. Since endothelial cells (ECs) regulate blood coagulation, their abnormal phenotype may play a role in the development of thrombotic events. We here aimed to investigate the effect of ponatinib on the procoagulant activity of cultured endothelial cells in vitro. Human coronary artery endothelial cells (HCAECs) were incubated with 50, 150, and 1000 nM of ponatinib. Subsequently, phosphatidylserine (PS) exposure and endothelial microvesicles (EMVs) were measured by flow cytometry. In addition, EC- and EMV-dependent thrombin generation was analyzed. To investigate pro-apoptotic effects of ponatinib, the level of Bax and Bcl-xL proteins were studied using Western blot and F3, THBD, and VCAM1 mRNAs were quantified by qPCR. Therapeutic concentrations of ponatinib significantly increased PS expression on ECs and the amount of EMVs which significantly shortened the time parameters of thrombin generation. In addition, these changes were associated with an increased ratio of Bax and Bcl-xL proteins in the presence of the decreased THBD mRNA level. Overall, ponatinib enhances the procoagulant activity of ECs via inducing apoptosis, which may contribute to thrombotic events.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ponatinib therapy
endothelial cell
apoptosis
phosphatidylserine
endothelial microvesicles
thrombin generation
Megjelenés:Pharmaceutics. - 16 : 4 (2024), p. 1-14. -
További szerzők:Pócsi Marianna (1989-) (klinikai laboratóriumi kutató) Fejes Zsolt (1988-) (molekuláris biológus) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Kappelmayer János (1960-) (laboratóriumi szakorvos) Bekéné Debreceni Ildikó (1970-) (biológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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