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001-es BibID:	BIBFORM068608
035-os BibID:	(cikkazonosító)9795271 (WOS)000402835500001 (Scopus)85021663462
Első szerző:	Hudák Renáta
Cím:	The phosphatase inhibitor calyculin-A impairs clot retraction, platelet activation and thrombin generation / Hudák Renáta, Vincze János, Csernoch László, Bekéné Debreceni Ildikó, Oláh Tamás, Erdődi Ferenc, Kenneth J. Clemetson, Kappelmayer János
Dátum:	2017
ISSN:	2314-6133 2314-6141
Megjegyzések:	The aim of this study was to investigate the effect of the serine/threonine protein phosphatase inhibitor, calyculin-A (CLA) on clot formation and on the procoagulant activity of human platelets. Platelet rich plasma (PRP) samples were preincubated with buffer or CLA and subsequently platelets were activated by the protease-activated receptor 1 (PAR-1) activator, thrombin-receptor activating peptide (TRAP). Clot retraction was detected by observing clot morphology up to 1 hour, phosphatidylserine (PS)-expression was studied by flow cytometry and thrombin generation was measured by a fluorimetric assay. For the intracellular Ca2+ assay, platelets were loaded with calcium-indicator dyes and the measurements were carried out using a ratiometric method with real-time confocal microscopy. CLA preincubation inhibited clot retraction, PS-expression and thrombin formation. TRAP activation elicited Ca2+ response and PS-expression in a subset of platelets. The activated PRP displayed significantly faster and enhanced thrombin generation compared to non-activated samples. CLA pretreatment abrogated PS-exposure and clot retraction also in TRAP-activated samples. As a consequence of the inhibitory effect on calcium elevation and PS-expression, CLA significantly downregulated thrombin generation in PRP. Our results show that CLA-pretreatment may be a useful tool to investigate platelet activation mechanisms that contribute to clot formation and thrombin generation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk phosphatases calyculin-A phosphatidylserine thrombin generation
Megjelenés:	Biomed Research International. - 2017 (2017), p. 1-10. -
További szerzők:	Vincze János (1988-) (orvos) Csernoch László (1961-) (élettanász) Bekéné Debreceni Ildikó (1970-) (biológus) Oláh Tamás (1983-) (élettanász) Erdődi Ferenc (1953-) (biokémikus) Clemetson, Kenneth J. Kappelmayer János (1960-) (laboratóriumi szakorvos)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM092257
035-os BibID:	(cikkazonosító)6642973 (WOS)000631875000006 (Scopus)85103189686
Első szerző:	Kis Adrienn (molekuláris biológus)
Cím:	In Vivo Molecular Imaging of the Efficacy of Aminopeptidase N (APN/CD13) Receptor Inhibitor Treatment on Experimental Tumors Using 68Ga-NODAGA-c(NGR) Peptide / Adrienn Kis, Noémi Dénes, Judit P. Szabó, Viktória Arató, Lívia Beke, Orsolya Matolay, Kata Nóra Enyedi, Gábor Méhes, Gábor Mező, Péter Bai, István Kertész, György Trencsényi
Dátum:	2021
ISSN:	2314-6133 2314-6141
Megjegyzések:	Introduction. The aminopeptidase N (APN/CD13) receptor plays an important role in the neoangiogenic process and metastatic tumor cell invasion. Clinical and preclinical studies reported that bestatin and actinonin are cytotoxic to APN/CD13-positive tumors and metastases due to their APN/CD13-specific inhibitor properties. Our previous studies have already shown that Ga-68-labeled NGR peptides bind specifically to APN/CD13 expressing tumor cells. The APN/CD13 specificity of Ga-68-NGR radiopharmaceuticals enables the following of the efficacy of antiangiogenic therapy with APN/CD13-specific inhibitors using positron emission tomography (PET). The aim of this in vivo study was to assess the antitumor effect of bestatin and actinonin treatment in subcutaneous transplanted HT1080 and B16-F10 tumor-bearing animal models using Ga-68-NODAGA-c(NGR). Materials and Methods. Three days after the inoculation of HT1080 and B16-F10 cells, mice were treated with intraperitoneal injection of bestatin (15 mg/kg) or actinonin (5 mg/kg) for 7 days. On the 5th and 10th day, in vivo PET scans and ex vivo biodistribution studies were performed 90 min after intravenous injection of 5.5 +/- 0.2 MBq(68)Ga-NODAGA-c(NGR). Results. Control-untreated HT1080 and B16-F10 tumors were clearly visualized by the APN/CD13-specific Ga-68-NODAGA-c(NGR) radiopharmaceutical. The western blot analysis also confirmed the strong APN/CDI3 positivity in the investigated tumors. We found significantly (p <= 0.05) lower radiopharmaceutical uptake after bestatin treatment and higher radiotracer accumulation in the actinonin-treated HT1080 tumors. In contrast, significantly lower (p <= 0.01) Ga-68-NODAGA-c(NGR) accumulation was observed in both bestatin- and actinonin-treated B16-F10 melanoma tumors compared to the untreated-control tumors. Bestatin inhibited tumor growth and Ga-68-NODAGA-c(NGR) uptake in both tumor models. Conclusion. The bestatin treatment is suitable for suppressing the neoangiogenic process and APN/CD13 expression of experimental HT1080 and B16-F10 tumors; furthermore, Ga-68-NODAGA-c(NGR) is an applicable radiotracer for the in vivo monitoring of the efficacy of the APN/CD13 inhibition-based anticancer therapies.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	BioMed Research International. - 2021 (2021), p. 1-11. -
További szerzők:	Dénes Noémi (1992-) (vegyész) Péli-Szabó Judit (1977-) (vegyész) Arató Viktória Zsófia (1989-) (gyógyszerész) Beke Lívia Matolay Orsolya (1989-) Enyedi Kata Nóra (1987-) (vegyész) Méhes Gábor (1966-) (patológus) Mező Gábor (1959-) (vegyész) Bai Péter (1976-) (biokémikus) Kertész István (1966-) (vegyész) Trencsényi György (1978-) (biológus, biokémikus, molekuláris biológus)
Pályázati támogatás:	NKFIH K119552 NKFIH NVKP_16-1-2016-0036 Egyéb EFOP-3.6.3-VEKOP-16-2017-00009 EFOP
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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