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001-es BibID:	BIBFORM064412
035-os BibID:	(scopus)84976324555 (wos)000381535900025
Első szerző:	Balogh Enikő (molekuláris biológus)
Cím:	Osteogenic differentiation of human lens epithelial cells might contribute to lens calcification / Enikő Balogh, Andrea Tóth, Emese Tolnai, Tímea Bodó, Emese Bányai, Dóra Júlia Szabó, Goran Petrovski, Viktória Jeney
Dátum:	2016
ISSN:	0006-3002
Megjegyzések:	Calcification of the human lens has been described in senile cataracts and in young patients with congenital cataractor chronic uveitis. Lens calcification is also a major complication of cataract surgery and plays a role in theopacification of intraocular lenses. A cell-mediated process has been suggested in the background of lens calcification,but so far the exact mechanism remained unexplored. Lens calcification shares remarkable similaritieswith vascular calcification; in both pathological processes hydroxyapatite accumulates in the soft tissue. Vascularcalcification is a regulated, cell-mediated process in which vascular cells undergo osteogenic differentiation. Ourobjective was to investigate whether human lens epithelial cells (HuLECs) can undergo osteogenic transitionin vitro, and whether this process contributes to lens calcification. We used inorganic phosphate (Pi) and Ca tostimulate osteogenic differentiation of HuLECs. Osteogenic stimuli (2.5 mmol/L Pi and 1.2 mmol/L Ca) inducedextracellular matrix mineralization and Ca deposition in HuLECswith the critical involvement of active Pi uptake.Osteogenic stimuli almost doubled mRNA expressions of osteo-/chondrogenic transcription factors Runx2 andSox9, which was accompanied by a 1.9-fold increase in Runx2 and a 5.5-fold increase in Sox9 protein expressions.Osteogenic stimuli induced mRNA and protein expressions of alkaline phosphatase and osteocalcin in HuLEC. Cacontentwas higher in human cataractous lenses, compared to non-cataractous controls (n=10). Osteocalcin, anosteoblast-specific protein, was expressed in 2 out of 10 cataractous lenses.We conclude that osteogenic stimuliinduce osteogenic differentiation of HuLECs and propose that this mechanism might play a role in lenscalcification.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Human lens epithelial cells Osteogenic differentiation Calcification Cataract Aging disease
Megjelenés:	Biochimica et Biophysica Acta (BBA). Molecular Basis of Disease. - 1862 : 9 (2016), p. 1724-1731. -
További szerzők:	Tóth Andrea (1992-) (molekuláris biológus) Szilágyi-Tolnai Emese (1988-) (Molekuláris biológus) Bodó Timea Bányai Emese (1984-) (orvos) Szabó Dóra Júlia (1985-) (Ph.D hallgató) Petrovski, Goran (1975-) (orvos) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:	K116024 OTKA RH/751-2/2015 Egyéb 4.2.2.A/2-11-1-2012-0001 TÁMOP KTIA_NAP_12-A_III/9 Egyéb
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001-es BibID:	BIBFORM055181
035-os BibID:	PMID: 25097723 Article ID: 976394
Első szerző:	Bányai Emese (orvos)
Cím:	Novel functional changes during podocyte differentiation : increase of oxidative resistance and H-ferritin expression / Emese Bányai, Enikő Balogh, Miklós Fagyas, Paolo Arosio, Zoltán Hendrik, Gábor Király, Gábor Nagy, Bence Tánczos, István Pócsi, György Balla, József Balla, Gáspár Bánfalvi, Viktória Jeney
Dátum:	2014
ISSN:	1942-0900 1942-0994
Megjegyzések:	Podocytes are highly specialized, arborized epithelial cells covering the outer surface of the glomerular tuft in the kidney. Terminally differentiated podocytes are unable to go through cell division and hereby they are lacking a key property for regeneration after a toxic injury. Podocytes are long-lived cells but, to date, little is known about the mechanisms that support their stress resistance. Our aim was to investigate whether the well-known morphological changes during podocyte differentiation are accompanied by changes in oxidative resistance in a manner that could support their long-term survival. We used a conditionally immortalized human podocyte cell line to study the morphological and functional changes during differentiation. We followed the differentiation process for 14 days by time-lapse microscopy. During this period nondifferentiated podocytes gradually transformed into large, nonproliferating, frequently multinucleated cells, with enlarged nuclei and opened chromatin structure. We observed that differentiated podocytes were highly resistant to oxidants such as H2O2 and heme when applied separately or in combination, whereas undifferentiated cells were prone to such challenges. Elevated oxidative resistance of differentiated podocytes was associated with increased activities of antioxidant enzymes and H-ferritin expression. Immunohistochemical analysis of normal human kidney specimens revealed that podocytes highly express H-ferritin in vivo as well.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Oxidative Medicine and Cellular Longevity 2014 (2014), p. 1-10. -
További szerzők:	Balogh Enikő (1987-) (molekuláris biológus) Fagyas Miklós (1984-) (orvos) Arosio, Paolo Hendrik Zoltán (1986-) (orvos) Király Gábor (1988-) (biológus) Szemán-Nagy Gábor (1975-) (biológia tanár-molekuláris biológus) Tánczos Bence (1987-) (biológus) Pócsi István (1961-) (vegyész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:	TÁMOP-4.2.2.A-11/1/KONV-2012-0045 TÁMOP Belgyógyászat Kutatócsoport TÁMOP-4.2.4.A/2-11-1-2012-0001 TÁMOP OTKA-K83478 OTKA
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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:	BIBFORM072211
035-os BibID:	(cikkazonosító)4310816 (PMID)29743981 (PMCID)PMC5883980
Első szerző:	Erdei Judit Zsuzsa (vegyész)
Cím:	Induction Of NLRP3 Inflammasome Activation By Heme In Human Endothelial Cells / Judit Erdei, Andrea Tóth, Enikő Balogh, Benard Bogonko Nyakundi, Emese Bányai, Bernhard Ryffel, György Paragh, Mario D. Cordero, Viktória Jeney
Dátum:	2018
ISSN:	1942-0994 1942-0900
Megjegyzések:	Hemolytic or hemorrhagic episodes are often associated with inflammation even when infectious agents are absent suggesting that red blood cells (RBCs) release damage-associated molecular patterns (DAMPs). DAMPs activate immune and nonimmune cells through pattern recognition receptors. Heme, released from RBCs, is a DAMP and induces IL-1β production through the activation of the nucleotide-binding domain and leucine-rich repeat-containing family and pyrin domain containing 3 (NLRP3) in macrophages; however, other cellular targets of heme-mediated inflammasome activation were not investigated. Because of their location, endothelial cells can be largely exposed to RBC-derived DAMPs; therefore, we investigated whether heme and other hemoglobin- (Hb-) derived species induce NLRP3 inflammasome activation in these cells. We found that heme upregulated NLRP3 expression and induced active IL-1β production in human umbilical vein endothelial cells (HUVECs). LPS priming largely amplified the heme-mediated production of IL-1β. Heme administration into C57BL/6 mice induced caspase-1 activation and cleavage of IL-1β which was not observed in NLRP3?/? mice. Unfettered production of reactive oxygen species played a critical role in heme-mediated NLRP3 activation. Activation of NLRP3 by heme required structural integrity of the heme molecule, as neither protoporphyrin IX nor iron-induced IL-1β production. Neither naive nor oxidized forms of Hb were able to induce IL-1β production in HUVECs. Our results identified endothelial cells as a target of heme-mediated NLRP3 activation that can contribute to the inflammation triggered by sterile hemolysis. Thus, understanding the characteristics and cellular counterparts of RBC-derived DAMPs might allow us to identify new therapeutic targets for hemolytic diseases.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Heme endothelial cells hemolysis hemoglobin DAMP NLRP3 inflammasome activation IL-1? ROS
Megjelenés:	Oxidative Medicine and Cellular Longevity. - 2018 (2018), p. 1-14. -
További szerzők:	Tóth Andrea (1992-) (molekuláris biológus) Balogh Enikő (1987-) (molekuláris biológus) Nyakundi, Benard Bogonko (1983-) (biokémikus) Bányai Emese (1984-) (orvos) Ryffel, Bernhard Paragh György (1953-) (belgyógyász) Cordero, Mario D. Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:	NKFIH K116024 Egyéb GINOP-2.3.2-15-2016-00005 GINOP
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