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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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2.

001-es BibID:BIBFORM025266
Első szerző:Jeney Viktória (vegyész, kémia tanár)
Cím:Ferritin/Ferroxidase Activity : a Potent Inhibitor of Vascular Calcification, Osteoblastic Transdifferentiation of Vascular Smooth Muscle Cells and Osteoblast Activity / Viktória Jeney, Abolfazl Zarjou, Paolo Arosio, Maura Poli, Anupam Agarwal, György Balla, József Balla
Dátum:2011
ISBN:978 1 61942 347 3
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
Megjelenés:Ferritin: Functions, Byosynthesis and Regulation / eds. Gael Soto da Lima, Marco F. Azevedo Cabral. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Arosio, Paolo Poli, Maura Agarwal, Anupam Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:TÁMOP-4.2.1./B-09/1/KONV-2010-0007
TÁMOP
Haemostasis thrombosis és vascularis biológia
OTKA-K75883
OTKA
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3.

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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4.

001-es BibID:BIBFORM077162
035-os BibID:(WoS)000457627800001 (Scopus)85062188852 (cikkazonosító)131
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Ferritin Light Chain Confers Protection Against Sepsis-Induced Inflammation and Organ Injury / Zarjou Abolfazl, Black Laurence M., McCullough Kayla R., Hull Travis D., Esman Stephanie K., Boddu Ravindra, Varambally Sooryanarayana, Chandrashekar Darshan S., Feng Wenguang, Arosio Paolo, Poli Maura, Balla Jozsef, Bolisetty Subhashini
Dátum:2019
ISSN:1664-3224
Megjegyzések:Despite the prevalence and recognition of its detrimental impact, clinical complications of sepsis remain a major challenge. Here, we investigated the effects of myeloid ferritin heavy chain (FtH) in regulating the pathogenic sequelae of sepsis. We demonstrate that deletion of myeloid FtH leads to protection against lipopolysaccharide-induced endotoxemia and cecal ligation and puncture (CLP)-induced model of sepsis as evidenced by reduced cytokine levels, multi-organ dysfunction and mortality. We identified that such protection is predominantly mediated by the compensatory increase in circulating ferritin (ferritin light chain; FtL) in the absence of myeloid FtH. Our in vitro and in vivo studies indicate that prior exposure to ferritin light chain restrains an otherwise dysregulated response to infection. These findings are mediated by an inhibitory action of FtL on NF-?B activation, a key signaling pathway that is implicated in the pathogenesis of sepsis. We further identified that LPS mediated activation of MAPK pathways, specifically, JNK, and ERK were also reduced with FtL pre-treatment. Taken together, our findings elucidate a crucial immunomodulatory function for circulating ferritin that challenges the traditional view of this protein as a mere marker of body iron stores. Accordingly, these findings will stimulate investigations to the adaptive nature of this protein in diverse clinical settings.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ferritin
inflammatory response
sepsis
NF-B, cytokine
LPS
multi-organ injury
myeloid cells
Megjelenés:Frontiers in Immunology. - 10 (2019), p. 1-15. -
További szerzők:Black, Laurence M. McCullough, Kayla R. Hull, Travis D. Esman, Stephanie K. Boddu, Ravindra Varambally, Sooryanarayana Chandrashekar, Darshan S. Feng, Wenguang Arosio, Paolo Poli, Maura Balla József (1959-) (belgyógyász, nephrológus) Bolisetty, Subhashini
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5.

001-es BibID:BIBFORM010279
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Ferritin ferroxidase activity : a potent inhibitor of osteogenesis / Abolfazl Zarjou, Viktória Jeney, Paolo Arosio, Maura Poli, Erzsébet Zavaczki, György Balla, József Balla
Dátum:2010
ISSN:0884-0431
Megjegyzések:Hemochromatosis is a known cause of osteoporosis, and iron overload has deleterious effects on bone. Although iron overload and its association with osteoporosis has long been recognized, the pathogenesis and exact role of iron have been undefined. Bone is an active tissue with constant remodeling capacity. Osteoblast (OB) development and maturation are under the influence of core binding factor alpha-1 (CBF-alpha1), which induces expression of OB-specific genes, including alkaline phosphatase, an important enzyme in early osteogenesis, and osteocalcin, a noncollagenous protein deposited within the osteoid. This study investigates the mechanism by which iron inhibits human OB activity, which in vivo may lead to decreased mineralization, osteopenia, and osteoporosis. We demonstrate that iron-provoked inhibition of OB activity is mediated by ferritin and its ferroxidase activity. We confirm this notion by using purified ferritin H-chain and ceruloplasmin, both known to possess ferroxidase activity that inhibited calcification, whereas a site-directed mutant of ferritin H-chain lacking ferroxidase activity failed to provide any inhibition. Furthermore, we are reporting that such suppression is not restricted to inhibition of calcification, but OB-specific genes such as alkaline phosphatase, osteocalcin, and CBF-alpha1 are all downregulated by ferritin in a dose-responsive manner. This study corroborates that iron decreases mineralization and demonstrates that this suppression is provided by iron-induced upregulation of ferritin. In addition, we conclude that inhibition of OB activity, mineralization, and specific gene expression is attributed to the ferroxidase activity of ferritin. 2010 American Society for Bone and Mineral Research
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Egészség- és Környezettudomány
Megjelenés:Journal of Bone and Mineral Research. - 25 : 1 (2010), p. 164-172. -
További szerzők:Jeney Viktória (1971-) (vegyész, kémia tanár) Arosio, Paolo Poli, Maura Zavaczki Erzsébet (1983-) (biotechnológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Újszülött-, és gyermekkori érbetegségek. A hemoxigenáznak és a ferritinnek, mint protektív stressz fehérjéknek szerepe intenzív ellátást igénylő újszülöttek és gyermekek akut és krónikus betegségeiben
OTKA-K75883
OTKA
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6.

001-es BibID:BIBFORM010063
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Ferritin prevents calcification and osteoblastic differentiation of vascular smooth muscle cells / Zarjou A., Jeney V., Arosio P., Poli M., Antal-Szalmas P., Agarwal A., Balla G., Balla J.
Dátum:2009
ISSN:1046-6673 (Print)
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of the American Society of Nephrology. - 20 : 6 (2009), p. 1254-1263. -
További szerzők:Jeney Viktória (1971-) (vegyész, kémia tanár) Arosio, Paolo Poli, Maura Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Agarwal, Anupam Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:OTKA-K75883
OTKA
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