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001-es BibID:	BIBFORM074228
Első szerző:	Fülöp Tibor (kardiológus)
Cím:	Adaptation of Vasomotor Function of Human Coronary Arterioles to the Simultaneous Presence of Obesity and Hypertension / Tibor Fulop, Eva Jebelovszki, Nora Erdei, Tamas Szerafin, Tamas Forster, Istvan Edes, Akos Koller, Zsolt Bagi
Dátum:	2007
ISSN:	1079-5642
Megjegyzések:	Objectives: We hypothesized that simultaneous presence of obesity and hypertension activates adaptive vascular mechanisms affecting dilations of human coronary arterioles.Methods and Results: Agonist-induced dilations were assessed in isolated pressurized coronary arterioles from patients(n 38) who underwent cardiac surgery. Among normotensives we found that dilations to bradykinin (BK) and the NO-donor, sodium-nitroprusside (SNP) were reduced in obese subjects (BK, 10 7 mol/L, lean:90 4%, obese:64 7%; SNP, 10 6 mol/L, lean:89 7%, obese:76 5%). However, among hypertensives, both BK- and SNP-induced dilations were significantly enhanced in obese patients, when compared with lean individuals (BK, lean:71 7%, obese:85 3%; SNP, lean:60 6%, obese:83 2%). Correspondingly, in hypertensive patients, but not in those of normotensives, a positive correlation was found between body mass index (BMI) and BK-induced (P 0.036, r 0.46), and also SNP-evoked (P 0.031, r 0.44) coronary dilations. Moreover, in additional 55 hypertensive patients flow-mediated (FMD) and nitroglycerin (NTG)-induced dilations of the brachial artery were assessed. In obese hypertensive individuals, FMD- and NTG-induced dilations were greater (FMD:6.2 0.7%, NTG:17.2 0.9%), than in leanhypertensive patients (FMD:3.7 0.6%, NTG:13.6 1.1%). Correspondingly, FMD- and NTG-induced dilations were positively correlated with BMI (P 0.020, r 0.31 and P 0.033, r 0.29, respectively).Conclusions:These findings are the first to suggest that obesity may lead to activation of adaptive vascular mechanisms to enhance the dilator function of coronary and peripheral arterial vessels in hypertensive patients. (Arterioscler Thromb Vasc Biol. 2007;27:2348-2354.)
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban obesity hypertension coronary microcirculation flow-mediated dilation nitrate
Megjelenés:	Arteriosclerosis Thrombosis And Vascular Biology. - 27 : 11 (2007), p. 2348-2354. -
További szerzők:	Jebelovszki Éva Erdei Nóra (1979-) (orvos) Szerafin Tamás (1960-) (szívsebész, mellkassebész) Forster Tamás Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:	F-048837 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM076938
035-os BibID:	(WoS)000460459200017 (Scopus)85062410676
Első szerző:	Sikura Katalin Éva (biológus)
Cím:	Potential Role of H-Ferritin in Mitigating Valvular Mineralization / Katalin Éva Sikura, László Potor, Tamás Szerafin, Abolfazl Zarjou, Anupam Agarwal, Paolo Arosio, Maura Poli, Zoltán Hendrik, Gábor Méhes, Melinda Oros, Niké Posta, Lívia Beke, Ibolya Fürtös, György Balla, József Balla
Dátum:	2019
ISSN:	1079-5642
Megjegyzések:	Objective- Calcific aortic valve disease is a prominent finding in elderly and in patients with chronic kidney disease. We investigated the potential role of iron metabolism in the pathogenesis of calcific aortic valve disease. Approach and Results- Cultured valvular interstitial cells of stenotic aortic valve with calcification from patients undergoing valve replacement exhibited significant susceptibility to mineralization/osteoblastic transdifferentiation in response to phosphate. This process was abrogated by iron via induction of H-ferritin as reflected by lowering ALP and osteocalcin secretion and preventing extracellular calcium deposition. Cellular phosphate uptake and accumulation of lysosomal phosphate were decreased. Accordingly, expression of phosphate transporters Pit1 and Pit2 were repressed. Translocation of ferritin into lysosomes occurred with high phosphate-binding capacity. Importantly, ferritin reduced nuclear accumulation of RUNX2 (Runt-related transcription factor 2), and as a reciprocal effect, it enhanced nuclear localization of transcription factor Sox9 (SRY [sex-determining region Y]-box 9). Pyrophosphate generation was also increased via upregulation of ENPP2 (ectonucleotide pyrophosphatase/phosphodiesterase-2). 3H-1, 2-dithiole-3-thione mimicked these beneficial effects in valvular interstitial cell via induction of H-ferritin. Ferroxidase activity of H-ferritin was essential for this function, as ceruloplasmin exhibited similar inhibitory functions. Histological analysis of stenotic aortic valve revealed high expression of H-ferritin without iron accumulation and its relative dominance over ALP in noncalcified regions. Increased expression of H-ferritin accompanied by elevation of TNF-α (tumor necrosis factor-α) and IL-1β (interleukin-1β) levels, inducers of H-ferritin, corroborates the essential role of ferritin/ferroxidase via attenuating inflammation in calcific aortic valve disease. Conclusions- Our results indicate that H-ferritin is a stratagem in mitigating valvular mineralization/osteoblastic differentiation. Utilization of 3H-1, 2-dithiole-3-thione to induce ferritin expression may prove a novel therapeutic potential in valvular mineralization.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk arteriosclerosis chronic kidney disease phosphate stenosis vascular calcification
Megjelenés:	Arteriosclerosis Thrombosis and Vascular Biology. - 39 : 3 (2019), p. 413-431. -
További szerzők:	Potor László Szerafin Tamás (1960-) (szívsebész, mellkassebész) Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Arosio, Paolo Poli, Maura Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Oros Melinda (1975-) (molekuláris biológus) Posta Niké Beke Lívia Fürtös Ibolya Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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