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001-es BibID:BIBFORM108774
035-os BibID:(cikkazonosító)102629 (WoS)000944336500001 (Scopus)85147884917
Első szerző:Combi Zsolt
Cím:Hydrogen sulfide as an anti-calcification stratagem in human aortic valve : altered biogenesis and mitochondrial metabolism of H2S lead to H2S deficiency in calcific aortic valve disease / Zsolt Combi, László Potor, Péter Nagy, Katalin Éva Sikura, Tamás Ditrói, Eszter Petra Jurányi, Klaudia Galambos, Tamás Szerafin, Péter Gergely, Matthew Whiteman, Roberta Torregrossa, Yuchao Ding, Lívia Beke, Zoltán Hendrik, Gábor Méhes, György Balla, József Balla
Dátum:2023
ISSN:2213-2317
Megjegyzések:Hydrogen sulfide (H2S) was previously revealed to inhibit osteoblastic differentiation of valvular interstitial cells (VICs), a pathological feature in calcific aortic valve disease (CAVD). This study aimed to explore the metabolic control of H2S levels in human aortic valves. Lower levels of bioavailable H2S and higher levels of interleukin-1? (IL-1?) and tumor necrosis factor-? (TNF-?) were detected in aortic valves of CAVD patients compared to healthy individuals, accompanied by higher expression of cystathionine ?-lyase (CSE) and same expression of cystathionine ?-synthase (CBS). Increased biogenesis of H2S by CSE was found in the aortic valves of CAVD patients which is supported by increased production of lanthionine. In accordance, healthy human aortic VICs mimic human pathology under calcifying conditions, as elevated CSE expression is associated with low levels of H2S. The expression of mitochondrial enzymes involved in H2S catabolism including sulfide quinone oxidoreductase (SQR), the key enzyme in mitochondrial H2S oxidation, persulfide dioxygenase (ETHE1), sulfite oxidase (SO) and thiosulfate sulfurtransferase (TST) were up-regulated in calcific aortic valve tissues, and a similar expression pattern was observed in response to high phosphate levels in VICs. AP39, a mitochondria-targeting H2S donor, rescued VICs from an osteoblastic phenotype switch and reduced the expression of IL-1? and TNF-? in VICs. Both pro-inflammatory cytokines aggravated calcification and osteoblastic differentiation of VICs derived from the calcific aortic valves. In contrast, IL-1? and TNF-? provided an early and transient inhibition of VICs calcification and osteoblastic differentiation in healthy cells and that effect was lost as H2S levels decreased. The benefit was mediated via CSE induction and H2S generation. We conclude that decreased levels of bioavailable H2S in human calcific aortic valves result from an increased H2S metabolism that facilitates the development of CAVD. CSE/H2S represent a pathway that reverses the action of calcifying stimu
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Arteriosclerosis
Chronic kidney disease
Hydrogen sulfide
Mitochondrial H(2)S catabolism
Phosphate
Valvular inflammation
Vascular calcification
Érelmeszesedés
Krónikus vesebetegség
Hidrogén-szulfid
Mitokondriális H(2)S katabolizmus
Foszfát
Valvuláris gyulladás
Vaszkuláris meszesedés
Megjelenés:Redox Biology. - 60 (2023), p. 1-19. -
További szerzők:Potor László Nagy Péter (1976-) (vegyész) Sikura Katalin Éva (1985-) (biológus) Ditrói Tamás (1989-) (vegyész) Jurányi Eszter Petra Galambos Klaudia (1995-) (biológus) Szerafin Tamás (1960-) (szívsebész, mellkassebész) Gergely Péter (1974-) (igazságügyi orvosszakértő) Whiteman, Matthew Torregrossa, Roberta Ding, Yuchao (1995-) (Ph.D. hallgató) Beke Lívia Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043 (IRONHEARTH)
GINOP
EFOP-3.6.2-16-2017-00006 (LIVE LONGER)
EFOP
TKP2020-NKA-04
Egyéb
TKP2021-EGA-18
Egyéb
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2.

001-es BibID:BIBFORM111320
035-os BibID:(cikkazonosító)102505 (WoS)000878597600003 (Scopus)85140235949
Első szerző:Czikora Ágnes (molekuláris biológus)
Cím:Cystathionine beta-synthase overexpression drives metastatic dissemination in pancreatic ductal adenocarcinoma via inducing epithelial-to-mesenchymal transformation of cancer cells / Ágnes Czikora, Katalin Erdélyi, Tamás Ditrói, Noémi Szantó, Eszter Petra Jurányi, Szilárd Szanyi, József Tóvári, Tamás Strausz, Péter Nagy
Dátum:2022
ISSN:2213-2317
Megjegyzések:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest of all cancer types with a constant rise in global incidence. Therefore, better understanding of PDAC biology, in order to design more efficient diagnostic and treatment modalities, is a priority.Here we found that the expression levels of cystathionine beta-synthase (CBS), a transsulfuration enzyme, is markedly elevated in metastatic PDAC cells compared to cell lines isolated from non-metastatic primary tumors. On human immunohistochemical samples from PDAC patients we also found higher CBS staining in cancerous ductal cells compared to in non-tumor tissue, which was further elevated in the lymph node metastasis of the same patients. In mice, orthotopically injected CBS-silenced T3M4 cells induced fewer liver metastases compared to control cells indicating important roles for CBS in PDAC cancer cell invasion and malignant transformation. Wound healing and colony formation assays in cell culture confirmed that CBS-deficient metastatic T3M4 and non-metastatic BxPC3 primary tumor cells migrate slower and have impaired anchorage-independent growth capacities compared to control T3M4 cells. CBS silencing in T3M4 cells lowered WNT5a and SNAI1 gene expression down to levels that were observed in BxPC3 cells as well as resulted in an increase in E-cadherin and a decrease in Vimentin signals in mouse tumors when injected orthotopically. These observations suggested a primary role for the epithelial to mesenchymal transformation of cancer cells in CBS-mediated tumor aggres-siveness. Under normal conditions, STAT3, an upstream regulator of Wnt signaling pathways, was less phos-phorylated and more oxidized in shCBS T3M4 and BxPC3 compared to control T3M4 cells, which is consistent with decreased transcriptional activity at lower CBS levels due to less protection against oxidation. Sulfur metabolome analyses suggested that this CBS-mediated protection against oxidative modifications is likely to be related to persulfide/sulfide producing activities of the enzyme rather than its canonical function to produce cystathionine for cysteine synthesis. Taken together, CBS overexpression through regulation of the EMT plays a significant role in PDAC cancer cell invasion and metastasis.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Hydrogen sulfide
Persulfide
Pancreatic ductal adenocarcinoma
Cystathionine beta-synthase
Epithelial-to-mesenchymal transition
Megjelenés:Redox Biology. - 57 (2022), p.1-14. -
További szerzők:Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Ditrói Tamás (1989-) (vegyész) Szántó Noémi Jurányi Eszter Petra Szanyi Szilárd Tóvári József Strausz Tamás Nagy Péter (1976-) (vegyész)
Pályázati támogatás:2022-2.1.1-NL-2022-00010
Egyéb
TKP2020-NKA-26
Egyéb
TKP2021-EGA-44
Egyéb
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3.

001-es BibID:BIBFORM111328
035-os BibID:(azonosító)P-210
Első szerző:Ditrói Tamás (vegyész)
Cím:Critical Re-Investigations of the Detection of Per-and Polysulfide Species in Cells for Metabolomic Measurements / Tamás Ditrói, Eszter Petra Jurányi, Klaudia Galambos, Péter Nagy
Dátum:2022
ISBN:9786155270741
Tárgyszavak:Orvostudományok Elméleti orvostudományok előadáskivonat
könyvrészlet
Megjelenés:33rd International Symposium on Chromatography - ISC 2022: Book of Abstracts / szerk. Felinger Attila. - p. 317.(P-210). -
További szerzők:Jurányi Eszter Petra Galambos Klaudia (1995-) (biológus) Nagy Péter (1976-) (vegyész)
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4.

001-es BibID:BIBFORM116150
035-os BibID:(cikkazonosító)16813 (WoS)001085340000073 (Scopus)85173792636
Első szerző:Orján Erik Márk
Cím:The anti-inflammatory effect of dimethyl trisulfide in experimental acute pancreatitis / Erik Márk Orján, Eszter Sára Kormányos, Gabriella Mihalekné Fűr, Ágnes Dombi, Emese Réka Bálint, Zsolt Balla, Beáta Adél Balog, Ágnes Dágó, Ahmad Totonji, Zoárd István Bátai, Eszter Petra Jurányi, Tamás Ditrói, Ammar Al-Omari, Gábor Pozsgai, Viktória Kormos, Péter Nagy, Erika Pintér, Zoltán Rakonczay, Lóránd Kiss
Dátum:2023
ISSN:2045-2322
Megjegyzések:Various organosulfur compounds, such as dimethyl trisulfide (DMTS), display anti-inflammatory properties. We aimed to examine the effects of DMTS on acute pancreatitis (AP) and its mechanism of action in both in vivo and in vitro studies. AP was induced in FVB/n mice or Wistar rats by caerulein, ethanol-palmitoleic acid, or L-ornithine-HCl. DMTS treatments were administered subcutaneously. AP severity was assessed by pancreatic histological scoring, pancreatic water content, and myeloperoxidase activity measurements. The behaviour of animals was followed. Pancreatic heat shock protein 72 (HSP72) expression, sulfide, and protein persulfidation were measured. In vitro acinar viability, intracellular Ca2+ concentration, and reactive oxygen species production were determined. DMTS dose-dependently decreased the severity of AP. It declined the pancreatic infiltration of leukocytes and cellular damage in mice. DMTS upregulated the HSP72 expression during AP and elevated serum sulfide and low molecular weight persulfide levels. DMTS exhibited cytoprotection against hydrogen peroxide and AP-inducing agents. It has antioxidant properties and modulates physiological but not pathophysiological Ca2+ signalling. Generally, DMTS ameliorated AP severity and protected pancreatic acinar cells. Our findings indicate that DMTS is a sulfur donor with anti-inflammatory and antioxidant effects, and organosulfur compounds require further investigation into this potentially lethal disease.
Tárgyszavak:Természettudományok Kémiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Scientific Reports. - 13 : 1 (2023), p. 1-19. -
További szerzők:Kormányos Eszter Sára Mihalekné Fűr Gabriella Dombi Ágnes Bálint Emese Réka Balla Zsolt Balog Beáta Adél Dágó Ágnes Totonji, Ahmad Bátai István Zoárd Jurányi Eszter Petra Ditrói Tamás (1989-) (vegyész) Al-Omari, Ammar Pozsgai Gábor Kormos Viktória Nagy Péter (1976-) (vegyész) Pintér Erika Rakonczay Zoltán Kiss Loránd (1974-) (vegyész)
Pályázati támogatás:EFOP-3.6.2-16-2017-00006
EFOP
GINOP-2.3.2-15-2016-00034
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5.

001-es BibID:BIBFORM116544
035-os BibID:(cikkazonosító)102368 (Scopus)85166745152 (WOS)001148470600001
Első szerző:Schilling, Danny
Cím:The influence of alkylating agents on sulfur-sulfur bonds in per- and polysulfides / Danny Schilling, Tamás Ditrói, Uladzimir Barayeu, Eszter Petra Jurányi, Peter Nagy, Tobias P. Dick
Dátum:2023
ISSN:1367-5931
Megjegyzések:Per- and polysulfides are sulfane sulfur species produced inside living cells, in organisms as diverse as bacteria, plants and humans, but their biological roles remain to be fully understood. Unfortunately, due to their reactivity, per- and polysulfides are easily altered, interconverted or lost during the processing and analysis of biological material. Thus, all current analytical methods make use of alkylating agents, to quench reactivity of hydropersulfides and hydropolysulfides and also to prevent free thiols from attacking sulfur chains in hydropolysulfides and dialkyl polysulfides. However, recent findings reveal that alkylating agents can also destroy per- and polysulfides, to varying degrees, depending on the choice of alkylating agent. Here, we discuss the challenges associated with the alkylation of per- and polysulfides, the single most important step for their preservation and detection in biological samples.
Tárgyszavak:Természettudományok Kémiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Hydropersulfides
Hydropolysulfides
Dialkyl polysulfides
Alkylating agents
Megjelenés:Current Opinion In Chemical Biology. - 76 (2023), p. 1-8. -
További szerzők:Ditrói Tamás (1989-) (vegyész) Barayeu, Uladzimir Jurányi Eszter Petra Nagy Péter (1976-) (vegyész) Dick, Tobias P.
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