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001-es BibID:BIBFORM067950
035-os BibID:(cikkazonosító)e0174585 (WOS)000399116700034 (Scopus)85016151227
Első szerző:Chen, Ji-Qing
Cím:MicroRNA expression profiles identify disease-specific alterations in systemic lupus erythematosus and primary Sjögren's syndrome / Ji-Qing Chen, Gábor Papp, Szilárd Póliska, Krisztina Szabó, Tünde Tarr, Bálint László Bálint, Péter Szodoray, Margit Zeher
Dátum:2017
ISSN:1932-6203
Megjegyzések:The discovery of microRNAs (miRNAs) and their critical role in genetic control opened new avenues in understanding of various biological processes including immune cell lineage commitment, differentiation, proliferation and apoptosis. However, a given miRNA may have hundreds of different mRNA targets and a target might be regulated by multiple miRNAs, thus the characterisation of dysregulated miRNA expression profiles could give a better insight into the development of immunological disturbances in autoimmune diseases. The aim of our study was to examine the changes in miRNA expression profiles in patients with systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (pSS). Eight SLE patients, 8 pSS patients and 7 healthy subjects were enrolled in the investigation. MiRNAs were isolated from peripheral blood mononuclear cells, and expression patterns were determined with Illumina next-generation sequencing technology. Since the immunopathogenesis of pSS and SLE encompasses pronounced B cell hyperactivity along with specific autoantibody production, we paid a special attention on the association between miRNA expression levels and altered peripheral B cell distribution. In SLE patients 135, while in pSS patients 26 miRNAs showed altered expression. Interestingly, the 25 miRNAs including miR-146a, miR-16 and miR-21, which were over-expressed in pSS patients, were found to be elevated in SLE group, as well. On the contrary, we observed the down-regulation of miR-150-5p, which is a novel and unique finding in pSS. Levels of several miRNAs over-expressed in SLE, were not changed in pSS, such as miR-148a-3p, miR-152, miR-155, miR-223, miR-224, miR-326 and miR-342. Expression levels of miR-223-5p, miR-150-5p, miR-155-5p and miR-342-3p, which miRNAs are potentially linked to B cell functions, showed associations with the B cell proportions within peripheral blood mononuclear cells. The observed differences in miRNA expression profiles and the better understanding of immune regulatory mechanisms of miRNAs may help to elucidate the pathogenesis of SLE and pSS.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
MicroRNA
systemic lupus erythematosus
primary Sjögren's syndrome
Megjelenés:PloS One. - 12 : 3 (2017), p. 1-32. -
További szerzők:Papp Gábor (1984-) (belgyógyász) Póliska Szilárd (1978-) (biológus) Szabó Krisztina (1987-) (Molekuláris biológus) Tarr Tünde (1976-) (belgyógyász, allergológus és klinikai immunológus) Bálint Bálint László (1971-) (kutató orvos) Szodoray Péter (1973-) (belgyógyász, orvos) Zeher Margit (1957-2018) (belgyógyász, allergológus és klinikai immunológus, reumatológus)
Pályázati támogatás:K-101470
OTKA
ÚNKP-16-4-III
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

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
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM064120
035-os BibID:(cikkazonosító)e0157651 (WOS)000378212400029 (Scopus)84976584488
Első szerző:Jóna Ádám (orvos)
Cím:Effect of bleomycin hydrolase gene polymorphism on late pulmonary complications of treatment for Hodgkin lymphoma / Ádám Jóna, Zsófia Miltényi, Szilárd Póliska, Bálint László Bálint, Árpád Illés
Dátum:2016
ISSN:1932-6203
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Plos One. - 11 : 6 (2016), p. e0157651. -
További szerzők:Miltényi Zsófia (1975-) (belgyógyász, haematológus) Póliska Szilárd (1978-) (biológus) Bálint Bálint László (1971-) (kutató orvos) Illés Árpád (1959-) (belgyógyász, haematológus, onkológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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4.

001-es BibID:BIBFORM074739
035-os BibID:(cikkazonosító)e0200840 (WOS)000439022400082 (Scopus)85050142161
Első szerző:Palkó Enikő (fül-orr-gégész)
Cím:Analysis of KRT1, KRT10, KRT19, TP53 and MMP9 expression in pediatric and adult cholesteatoma / Palkó Enikő, Póliska Szilárd, Sziklai István, Penyige András
Dátum:2018
ISSN:1932-6203
Megjegyzések:Cholesteatoma is an epidermal cyst with still unknown pathomechanism. The aim of the current study was to investigate molecular differences in the background of the hyperproliferative property and aggressive behavior typical of the cholesteatoma epithelium. The expression of three cytokeratin genes (KRT1, KRT10 and KRT19), the matrix metalloproteinase 9 gene (MMP9) and the tumor suppressor TP53 gene was measured by qRT-PCR in surgical samples of pediatric and adult cholesteatoma cases and their expression level was compared to that of normal skin samples from the retroauricular region of control individuals. Cholesteatoma samples were stratified according to the age of onset and recurrence for more detailed analysis. Our results showed identical expression pattern for KRT1 and KRT10, their expression was higher in pediatric cases than in adults, especially in pediatric recurrent samples. The expression level of KRT19 was inversely proportional to that of KRT1/KRT10, it was lower in the more invasive recurrent cases both in our pediatric and adult groups. As it was expected from the bone destructive behavior of cholesteatoma, a significantly elevated expression of MMP9 was measured in cholesteatoma samples, the highest level was found in adult recurrent cases. Low expression levels characterize the TP53 gene without significant differences in our samples. These findings demonstrate that cytokeratin expression distinguishes between pediatric/adult, nonrecurrent/recurrent cases, suggesting that distinct differentiation state and cell division potential characterize these cholesteatoma cases. KRT19 with a tumor suppressor potential might restrict the recurrence of cholesteatoma. The differences observed in gene expression profiles between cholesteatoma and control samples support the notion that cholesteatoma is a cystic lesion with tumor-like behavior because it is characterized by invasive, destructive growth and high tendency for recurrence.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
KRT1
KRT10
TP53
MMP9
Megjelenés:Plos One. - 13 : 7 (2018), p. 1-12. -
További szerzők:Póliska Szilárd (1978-) (biológus) Sziklai István (1954-) (fül-orr-gégész) Penyige András (1954-) (molekuláris genetikus)
Pályázati támogatás:K81480
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM074734
035-os BibID:(cikkazonosító)e0198323 (WOS)000435802500016 (Scopus)85048863741
Első szerző:Töröcsik Dániel (bőrgyógyász)
Cím:Genome wide analysis of TLR1/2- and TLR4-activated SZ95 sebocytes reveals a complex immune-competence and identifies serum amyloid A as a marker for activated sebaceous glands / Dániel Törőcsik, Dóra Kovács, Szilárd Póliska, Zita Szentkereszty-Kovács, Marianna Lovászi, Katalin Hegyi, Andrea Szegedi, Christos C. Zouboulis, Mona Ståhle
Dátum:2018
ISSN:1932-6203
Megjegyzések:Toll-like receptors (TLR) 2 and 4 are active in sebaceous glands and play a central role in the development of acne. Still, there is only limited knowledge on their effect on sebocytes. In this work we performed global gene expression profile analysis with functional clustering of the differentially regulated genes of TLR1/2 (PAM3CSK4)- and TLR4 (lipopolysaccharide [LPS])-activated SZ95 sebocytes. Both TLR1/2- and 4-activation promoted inflammation in a similar manner already at an early time-point (6 hours), regulating genes involved in inflammation, wound healing and chemotaxis reflecting a more complex cytokine and chemokine regulation than previously known. Importantly, lipid metabolism, the primary feature of sebocytes, was affected at the level of gene expression only at a later time point (24 hours) indicating that sebocytes prioritize to exert a pro-inflammatory phenotype when confronted with a danger signal. Supporting the biological relevance of our results, a meta-analysis revealed that the genes showing the strongest up-regulation were also found up-regulated in acne. Of these genes, serum amyloid A 1/2 (SAA1/2) was confirmed to be a suitable protein marker for in vivo activated sebocytes, underlining their immune-competence, which is structurally defined within sebaceous glands of acne and rosacea skin samples. Altogether our findings demonstrate that sebocytes are not only positioned at the end point of inflammation but are actively involved in shaping the inflammatory response with putative diagnostic and therapeutic relevance.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Acne
Gene expression
Sebaceous glands
Inflammation
Gene regulation
Inflammatory diseases
Immune response
Lipid metabolism
Megjelenés:Plos One. - 13 : 6 (2018), p. 1-20. -
További szerzők:Kovács Dóra (1988-) (Biológus) Póliska Szilárd (1978-) (biológus) Szentkereszty-Kovács Zita (1988-) (orvos) Lovászi Marianna (1986-) (biológus) Dull Katalin (1983-) (molekuláris biológus, genetikus) Szegedi Andrea (1964-) (bőrgyógyász) Zouboulis, Christos C. (1960-) (bőrgyógyász) Ståhle, Mona
Pályázati támogatás:GINOP-2.3.2-15-2016-00005
GINOP
GINOP-2.3.2-15-2016-00050
GINOP
EFOP-3.6.1-16-2016-00022
EFOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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