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001-es BibID:	BIBFORM061878
Első szerző:	Becs Gergely
Cím:	Pharmacological induction of ferritin prevents osteoblastic transformation of smooth muscle cells / Gergely Becs, Abolfazl Zarjou, Anupam Agarwal, Katalin Éva Kovács, Ádám Becs, Mónika Nyitrai, Enikő Balogh, Emese Bányai, John W. Eaton, Paolo Arosio, Maura Poli, Viktória Jeney, József Balla, György Balla
Dátum:	2016
ISSN:	1582-1838
Megjegyzések:	Vascular calcification is a frequent complication of atherosclerosis, diabetes and chronic kidney disease. In the latter group of patients, calcification is commonly seen in tunica media where smooth muscle cells (SMC) undergo osteoblastic transformation. Risk factors such as elevated phosphorus levels and vitamin D3 analogues have been identified. In the light of earlier observations by our group and others, we sought to inhibit SMC calcification via induction of ferritin. Human aortic SMC were cultured using b-glycerophosphate with activated vitamin D3, or inorganic phosphate with calcium, and induction of alkaline phosphatase (ALP) and osteocalcin as well as accumulation of calcium were used to monitor osteoblastic transformation. In addition, to examine the role of vitamin D3 analogues, plasma samples from patients on haemodialysis who had received calcitriol or paricalcitol were tested for their tendency to induce calcification of SMC. Addition of exogenous ferritin mitigates the transformation of SMC into osteoblast-like cells. Importantly, pharmacological induction of heavy chain ferritin by 3H-1,2-Dithiole-3-thione was able to inhibit the SMC transition into osteoblast-like cells and calcification of extracellular matrix. Plasma samples collected from patients after the administration of activated vitamin D3 caused significantly increased ALP activity in SMC compared to the samples drawn prior to activated vitamin D3 and here, again induction of ferritin diminished the osteoblastic transformation. Our data suggests that pharmacological induction of ferritin prevents osteoblastic transformation of SMC. Hence, utilization of such agents that will cause enhanced ferritin synthesis may have important clinical applications in prevention of vascular calcification.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban ferritin ferroxidase activity [béta]-glycerophosphate vascular calcification vitamin D3
Megjelenés:	Journal Of Cellular And Molecular Medicine. - 20 : 2 (2016), p. 217-230. -
További szerzők:	Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Sikura Katalin Éva (1985-) (biológus) Becs Ádám Nyitrai Mónika Balogh Enikő (1987-) (molekuláris biológus) Bányai Emese (1984-) (orvos) Eaton, John W. Arosio, Paolo Poli, Maura Jeney Viktória (1971-) (vegyész, kémia tanár) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
Pályázati támogatás:	TÁMOP-4.2.2.A-11/1/KONV-2012-0045 TÁMOP Belgyógyászat Kutatócsoport K-112333(B.J.) OTKA MTA-DE MTA Vascularis Biológia, Thrombosis-Haemostasis Kutatócsoport
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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)
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