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001-es BibID:	BIBFORM120915
035-os BibID:	(Scopus)85125965764 (WoS)000743142600029
Első szerző:	Akhmedov, Alexander
Cím:	TNFα induces endothelial dysfunction in rheumatoid arthritis via LOX-1 and Arginase 2 : reversal by monoclonal TNFα antibodies / Alexander Akhmedov, Margot Crucet, Branko Simic, Simon Kraler, Nicole R. Bonetti, Caroline Ospelt, Oliver Distler, Adrian Ciurea, Luca Liberale, Matti Jauhiainen, Jari Metso, Melroy Miranda, Rose Cydecian, Lena Schwarz, Vera Fehr, Rita Zilinyi, Mohammad Amrollahi-Sharifabadi, Lydia Ntari, Niki Karagianni, Frank Ruschitzka, Reijo Laaksonen, Paul M. Vanhoutte, George Kollias, Giovanni G. Camici, Thomas F. Lüscher
Dátum:	2022
ISSN:	0008-6363
Megjegyzések:	Aims: Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting joints and blood vessels. Despite low levels of low-density lipoprotein cholesterol (LDL-C), RA patients exhibit endothelial dysfunction and are at increased risk of death from cardiovascular complications, but the molecular mechanism of action is unknown. We aimed in the present study to identify the molecular mechanism of endothelial dysfunction in a mouse model of RA and in patients with RA. Methods and results: Endothelium-dependent relaxations to acetylcholine were reduced in aortae of two tumour necrosis factor alpha (TNF?) transgenic mouse lines with either mild (Tg3647) or severe (Tg197) forms of RA in a time-and severity-dependent fashion as assessed by organ chamber myograph. In Tg197, TNF? plasma levels were associated with severe endothelial dysfunction. LOX-1 receptor was markedly up-regulated leading to increased vascular oxLDL uptake and NF?B-mediated enhanced Arg2 expression via direct binding to its promoter resulting in reduced NO bioavailability and vascular cGMP levels as shown by ELISA and chromatin immunoprecipitation. Anti-TNF? treatment with infliximab normalized endothelial function together with LOX-1 and Arg2 serum levels in mice. In RA patients, soluble LOX-1 serum levels were also markedly increased and closely related to serum levels of C-reactive protein. Similarly, ARG2 serum levels were increased. Similarly, anti-TNF? treatment restored LOX-1 and ARG2 serum levels in RA patients. Conclusions: Increased TNF? levels not only contribute to RA, but also to endothelial dysfunction by increasing vascular oxLDL content and activation of the LOX-1/NF?B/Arg2 pathway leading to reduced NO bioavailability and decreased cGMP levels. Anti-TNF? treatment improved both articular symptoms and endothelial function by reducing LOX-1, vascular oxLDL, and Arg2 levels. ? 2021 Published on behalf of the European Society of Cardiology. All rights reserved.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Arg2 Endothelium LOX-1 Rheumatoid arthritis TNFα
Megjelenés:	Cardiovascular Research. - 118 : 1 (2022), p. 254-266. -
További szerzők:	Crucet, Margot Simic, Branko Kraler, Simon Bonetti, Nicole R. Ospelt, Caroline Distler, Oliver Ciurea, Adrian Liberale, Luca Jauhiainen, Matti Metso, Jari Miranda, Melroy Cydecian, Rose Schwarz, Lena Fehr, Vera Zilinyi Rita (1990-) (Klinikai laboratóriumi kutató) Amrollahi-Sharifabadi, Mohammad Ntari, Lydia Karagianni, Niki Ruschitzka, Frank Laaksonen, Reijo Vanhoutte, Paul M. Kollias, George Camici, Giovanni G. Lüscher, Thomas F.
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001-es BibID:	BIBFORM004074
Első szerző:	Birinyi Péter (élettanász)
Cím:	The Na+/Ca2+ exchange blocker SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in canine ventricular cardiomyocytes / Birinyi P., Tóth A., Jóna I., Acsai K., Almássy J., Nagy N., Prorok J., Gherasim I., Papp Z., Hertelendi Z., Szentandrássy N., Bányász T., Fülöp F., Papp J. G., Varró A., Nánási P. P., Magyar J.
Dátum:	2008
Megjegyzések:	Aims This study was designed to evaluate the effects of the Na+/Ca2+ exchange (NCX) inhibitor SEA0400 on Ca2+ handling in isolated canine ventricular myocytes. Methods and results Intracellular Ca2+ ([Ca2+](i)) transients, induced by either field stimulation or caffeine flush, were monitored using Ca2+ indicator dyes. [Ca2+](i)-dependent modulation of the inhibitory effect of SEA0400 on NCX was characterized by the changes in Ni2+-sensitive current in voltage-clamped myocytes. Sarcoplasmic reticulum (SR) Ca2+ release and uptake were studied in SIR membrane vesicles. Gating properties of single-ryanodine receptors were analysed in lipid bilayers. Ca2+ sensitivity of the contractile machinery was evaluated in chemically skinned myocytes. In myocytes paced at 1 Hz, neither diastolic [Ca2+](i) nor the amplitude of [Ca2+](i) transients was significantly altered by SEA0400 up to the concentration of 1 mu M, which was shown to inhibit the exchange current. The blocking effect of SEA0400 on NCX decreased with increasing [Ca2+](i), and it was more pronounced in reverse than in forward mode operation at every [Ca2+](i) examined. The rate of decay of the caffeine-induced [Ca2+](i) transients was decreased significantly by 1 mu M SEA0400; however, this effect was only a fraction of that observed with 10 mM NiCl2. Neither SR Ca2+ release and uptake nor cell shortening and Ca2+ sensitivity of the contractile proteins were influenced by SEA0400. Conclusion The lack of any major SEA0400-induced shift in Ca2+ transients or contractility of myocytes can well be explained by its limited inhibitory effect on NCX (further attenuated by elevated [Ca2+](i) levels) and a concomitant reduction in Ca2+ influx due to the predominantly reverse mode blockade of NCX and suppression of L-type Ca2+ current.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Cardiovascular Research. - 78 : 3 (2008), p. 476-484. -
További szerzők:	Tóth András (farmakológus) Jóna István (1948-) (élettanász, fizikus) Acsai Károly Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Nagy Norbert (1977-) (kísérletes farmakológus) Prorok János Gherasim, Iuliana Papp Zoltán (1965-) (kardiológus, élettanász) Hertelendi Zita (1978-) (orvos) Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Fülöp Ferenc Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász)
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001-es BibID:	BIBFORM014453
Első szerző:	Gurusamy, Narasimman
Cím:	Cardioprotection by resveratrol : a novel mechanism via autophagy involving the mTORC2 pathway / Narasimman Gurusamy, Istvan Lekli, Subhendu Mukherjee, Diptarka Ray, Md. Kaimul Ahsan, Mihaela Gherghiceanu, Lawrence M. Popescu, Dipak K. Das
Dátum:	2010
ISSN:	0008-6363
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Cardiovascular Research. - 86 : 1 (2010), p. 103-112. -
További szerzők:	Lekli István (1981-) (gyógyszerész) Mukherjee, Subhendu Ray, Diptarka Ahsan, Md. Kaimul Gherghiceanu, Mihaela Popescu, Laurenciu M. Das, Dipak Kumar
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