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1.

001-es BibID:BIBFORM066281
Első szerző:Balogh Enikő (molekuláris biológus)
Cím:Impaired Immunosuppressive Effect of Bronchoalveolar Mesenchymal Stem Cells in Hypersensitivity Pneumonitis : preliminary findings / Eniko Balogh, Bela Nagy Jr., Agnes Gyetvai, Zsolt Bene, Zoltan Hendrik, Viktoria Jeney, Peter Nagy, Agnes Papp, Jozsef Balla, Gyorgy Balla, Janos Kappelmayer, Bela Nagy
Dátum:2018
ISSN:1552-4949
Megjegyzések:Bronchoalveolar mesenchymal stem cells (MSCs) play an important role in the maintenance of lung integrity. Therapeutic application of bone marrow-derived MSCs reduced chronic bronchial inflammation in idiopathic pulmonary fibrosis, and improved the ratio of survivors in sepsis with pneumonia. This study investigated the effect of MSCs from bronchoalveolar lavage fluid (BALF) of hypersensitivity pneumonitis (HP) on T-cell function under in vitro conditions.METHODS:Bronchoalveolar MSCs were obtained via bronchoscopy with BAL from children with severe subacute HP. As control, BALF MSCs were assessed from children without any inflammatory lung disease. Isolated MSCs were characterized via immunophenotyping by flow cytometry and confocal laser scanning microscopy. HP-derived and healthy separated peripheral blood mononuclear cells (PBMCs) were stimulated by 5 ?g/mL phytohemagglutinin in the presence of HP-derived or control MSCs in 5-day cultures. Proliferation and activation of T-cells were characterized by the mean fluorescence intensity (MFI) of 5,6-carboxyfluorescein-diacetat succinimidyl ester (CFSE) and CD25, CD69 as well as HLA-DR surface positivities, respectively.RESULTS:HP-derived MSCs showed significantly lower level of CD73, CD90, and CD105 expression compared to control MSCs in both flow cytometric and confocal microscopic experiments. MSCs from HP did not reduce T-cell proliferation based on CFSE MFI values, while the level of CD25 expression on both control and HP-derived CD4+ and CD8+ T-cells was significantly reduced by normal MSCs, while HP-derived MSCs did not have any significant effect. The level of other activation markers was not markedly modulated by MSCs.CONCLUSIONS:BALF MSCs from HP are unable to downregulate the proliferation and activation of T-cells that may support the development of recurrent intrapulmonary inflammation in HP. ? 2016 Clinical Cytometry Society.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
T-lymphocyte proliferation and activation
bronchoalveolar lavage
hypersensitivity pneumonitis
mesenchymal stem cells
Megjelenés:Cytometry Part B-Clinical Cytometry. - 94 : 2 (2018), p. 363-368. -
További szerzők:Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Gyetvai Ágnes Bene Zsolt (1981-) (orvos) Hendrik Zoltán (1986-) (orvos) Jeney Viktória (1971-) (vegyész, kémia tanár) Nagy Péter (1971-) (biofizikus) Papp Ágnes (1967-) (gyermekgyógyász, pulmonológus) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Nagy Béla (1949-) (csecsemő- és gyermekgyógyász, gyermek-tüdőgyógyász)
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2.

001-es BibID:BIBFORM064368
035-os BibID:(scopus)84973487274 (wos)000381535900018
Első szerző:Balogh Enikő (molekuláris biológus)
Cím:Iron overload inhibits osteogenic commitment and differentiation of mesenchymal stem cells via the induction of ferritin / Enikő Balogh, Emese Tolnai, Béla Nagy, Jr. Béla Nagy, György Balla, József Balla, Viktória Jeney
Dátum:2016
ISSN:0925-4439
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Biochimica et Biophysica Acta (BBA). Molecular Basis of Disease. - 1862 : 9 (2016), p. 1640-1649. -
További szerzők:Szilágyi-Tolnai Emese (1988-) (Molekuláris biológus) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Nagy Béla (1949-) (csecsemő- és gyermekgyógyász, gyermek-tüdőgyógyász) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:OTKA-K116024
OTKA
TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
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3.

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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4.

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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5.

001-es BibID:BIBFORM074180
035-os BibID:(cikkazonosító)e0197890 (WOS)000434786600008 (Scopus)85048322440
Első szerző:Fejes Zsolt (molekuláris biológus)
Cím:Endothelial cell activation is attenuated by everolimus via transcriptional and post-transcriptional regulatory mechanisms after drug-eluting coronary stenting / Fejes Z., Czimmerer Z., Szük T., Póliska S., Horváth A., Balogh E., Jeney V., Váradi J., Fenyvesi F., Balla G., Édes I., Balla J., Kappelmayer J., Nagy B. Jr.
Dátum:2018
ISSN:1932-6203
Megjegyzések:We previously found higher level of endothelial cell (EC) activation in patients who suffered from in-stent restenosis after bare-metal stenting compared to subjects who underwent drug-eluting stenting (DES) showing no complications. Here we investigated the potential transcriptional and post-transcriptional regulatory mechanisms by which everolimus attenuated EC activation after DES. We studied the effect of everolimus on E-selectin (SELE) and VCAM1 mRNA levels when human coronary artery (HCAECs) and human umbilical vein ECs were challenged with recombinant TNF-? (100 ng/mL) for 1-24 hours in the presence or absence of everolimus using 0.5 ?M concentration locally maintained by DES. EC activation was evaluated via the levels of IL-1? and IL-6 mRNAs with miR-155 expression by RT-qPCR as well as the nuclear translocation of nuclear factor kappa beta (NF-?B) detected by fluorescence microscopy. To investigate the transcriptional regulation of E-selectin and VCAM-1, TNF-?-induced enhancer RNA (eRNA) expression at p65-bound enhancers in the neighboring genomic regions of SELE and VCAM1 genes, including SELE_-11Kb and VCAM1_-10Kb, were measured in HCAECs. Mature and precursor levels of E-selectin and VCAM-1 repressor miR-181b were quantified to analyze the post-transcriptional regulation of these genes in HCAECs. Circulating miR-181b was analyzed in plasma samples of stented subjects by stem-loop RT-qPCR. TNF-? highly elevated E-selectin and VCAM-1 expression at transcriptional level in ECs. Levels of mature, pre- and pri-miR-181b were repressed in ECs by TNF-?, while everolimus acted as a negative regulator of EC activation via inhibited translocation of NF-?B p65 subunit into cell nuclei, lowered eRNA expression at SELE and VCAM1 genes-associated enhancers and modulated expression of their post-transcriptional repressor miR-181b. Significant negative correlation was observed between plasma miR-181b and soluble E-selectin and VCAM-1 in patients. In conclusion, everolimus attenuates EC activation via reduced NF-?B p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
coronary stenting
endothelial cell
enhancer RNA
everolimus
inflammation
microRNA
Megjelenés:Plos One. - 13 : 6 (2018), p. 1-20. -
További szerzők:Czimmerer Zsolt (1981-) (molekuláris biológus) Szűk Tibor (1967-) (kardiológus) Póliska Szilárd (1978-) (biológus) Horváth Attila (1988-) (programtervező informatikus) Balogh Enikő (1987-) (molekuláris biológus) Jeney Viktória (1971-) (vegyész, kémia tanár) Váradi Judit (1973-) (gyógyszerész, gyógyszertechnológus) Fenyvesi Ferenc (1977-) (gyógyszerész, gyógyszertechnológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Édes István (1952-) (kardiológus) Balla József (1959-) (belgyógyász, nephrológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
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6.

001-es BibID:BIBFORM071326
Első szerző:Potor László
Cím:Hydrogen Sulfide Abrogates Hemoglobin-Lipid Interaction In Atherosclerotic Lesion / László Potor, Peter Nagy, Gabor Méhes, Zoltán Hendrik, Viktória Jeney, Dávid Pethő, Anita Vasas, Zoltán Pálinkás, Enikő Balogh, Ágnes Gyetvai, Matthew Whiteman, Roberta Torregrossa, Mark E. Wood, Sándor Olvasztó, Péter Nagy, György Balla, József Balla
Dátum:2018
ISSN:1942-0994 1942-0900
Megjegyzések:The infiltration of red blood cells into atheromatous plaques is implicated in atherogenesis. Inside the lesion hemoglobin (Hb) is oxidized to ferri- and ferrylHb which exhibit pro-oxidant and pro-inflammatory activities. Cystathione-gamma lyase (CSE)-derived H2S has been suggested to possess various anti-atherogenic actions.Expression of CSE was upregulated predominantly in macrophages, foam cells and myofibroblasts of human atherosclerotic lesions derived from carotid artery specimens of patients. Similar pattern was observed in aortic lesions of apolipoprotein E deficient mice on high-fat diet. We identified several triggers for inducing CSE expression in macrophages and vascular smooth muscle cells including heme, ferrylHb, plaque lipids, oxidized low-density lipoprotein, tumor necrosis factor-? and interleukin-1?. In the interplay between hemoglobin and atheroma lipids, H2S significantly mitigated oxidation of Hb preventing the formation of ferrylHb derivatives, therefore providing a novel function as a heme-redox-intermediate-scavenging antioxidant. By inhibiting Hb-lipid interactions sulfide lowered oxidized Hb-mediated induction of adhesion molecules in endothelium and disruption of endothelial integrity. Exogenous H2S inhibited heme and Hb-mediated lipid oxidation of human atheroma derived lipid and human complicated lesion.Our study suggests that the CSE/H2S system represents an atheroprotective pathway for removing or limiting the formation of oxidized Hb and lipid derivatives in the atherosclerotic plaque.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
CSE expression
Hb-lipid interactions
CSE/H2S system
Megjelenés:Oxidative Medicine and Cellular Longevity. - 2018 (2018), p. 1-16. -
További szerzők:Nagy Péter Méhes Gábor (1966-) (patológus) Hendrik Zoltán (1986-) (orvos) Jeney Viktória (1971-) (vegyész, kémia tanár) Pethő Dávid Vasas Anita (1987-) (környezetkutató) Pálinkás Zoltán (1984-) (vegyész) Balogh Enikő (1987-) (molekuláris biológus) Gyetvai Ágnes Whiteman, Matthew Torregrossa, Roberta Wood, Mark E. Olvasztó Sándor (1957-) (sebész) Nagy Péter (1976-) (vegyész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:K112333
OTKA
K109843
OTKA
K116024
OTKA
TÁMOP 4.2.4.A/2-11/1-2012-0001
TÁMOP
TÁMOP 4.2.4.A/2-11/1- 2012-0001
TÁMOP
EFOP-3.6.2-16-2017-00006
Egyéb
GINOP-2.3.2-15-2016-00043
GINOP
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