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001-es BibID:	BIBFORM020146
Első szerző:	Altorjay István (belgyógyász, gasztroenterológus, onkológus)
Cím:	Anti-TNF-alpha antibody (infliximab) therapy supports the recovery of eNOS and VEGFR2 protein expression in endothelial cells / Istvan Altorjay, Zoltan Vereb, Zoltan Serfozo, Ildiko Bacskai, Robert Batori, Ferenc Erdodi, Miklos Udvardy, Sandor Sipka, Arpad Lanyi, Eva Rajnavolgyi, Karoly Palatka
Dátum:	2011
Megjegyzések:	The aim of this study is to investigate the effect of sera obtained from patients of Crohn's disease treated by anti-TNF-alpha antibody (infliximab) on the expression of endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor receptor-2 (VEGFR2) protein in human umbilical vein endothelial cells (HUVEC) cultured in vitro. HUVEC was cultured in the presence of sera derived from patients before and after treatment, or from healthy individuals. Effects of sera on the expression of eNOS and VEGFR2 were monitored by determination of mRNA and protein levels using real time quantitative PCR and Western blot analysis, respectively. The serum of Crohn's patients contained elevated levels of TNF-alpha (34 +/- 1.80 pg/mL), which resulted in a decrease in the protein level of eNOS in HUVEC with a simultaneous induction of VEGFR2. Infliximab treatment normalized the expression level of these proteins by decreasing TNF-alpha level, particularly in those cases when clinical healing was also recorded, and it also conferred restitution of the level of angiogenic cytokines. Results suggest that altered angiogenesis possibly contributes to the initiation and perpetuation of inflammatory processes in Inflammatory Bowel Disease (IBD). Endothelial dysfunction, a selective feature of Crohn's disease is beneficially affected by intravascular TNF-alpha neutralization.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Crohn's disease eNOS HUVEC inflammatory bowel disease infliximab TNF-alpha Vascular endothelial growth factor receptor-2
Megjelenés:	International Journal of Immunopathology and Pharmacology 24 : 2 (2011), p. 323-335. -
További szerzők:	Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Serfőző Zoltán Bacskai Ildikó (1985-) (immunológus) Bátori Róbert Károly (1983-) (biológus, biotechnológus) Erdődi Ferenc (1953-) (biokémikus) Udvardy Miklós (1947-) (belgyógyász, haematológus) Sipka Sándor (1945-) (laboratóriumi szakorvos) Lányi Árpád (1962-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Palatka Károly (1961-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:	0046/NA/2006-2/OP-9 Egyéb
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM037289
Első szerző:	Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:	Temporally designed treatment of melanoma cells by ATRA and polyI:C results in enhanced chemokine and IFNb secretion controlled differently by TLR3 and MDA5 / Szabo Attila, Osman Rolah M., Bacskai Ildiko, Kumar Brahma V., Agod Zsofia, Lanyi Arpad, Gogolak Peter, Rajnavolgyi Eva
Dátum:	2012
ISSN:	0960-8931
Megjegyzések:	In the last three decades, the incidence of melanoma has increased worldwide and no effective treatment modalities have been developed yet. All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. We addressed the question of whether ATRA pretreatment could enhance the efficacy of polyI:C and, if so, would ATRA have any additional effects on this process. We found that the combined treatment of human melanoma cells with ATRA and polyI:C strongly increased the expression of TLR3 and MDA5 in both WM35 and WM983A cells associated with significantly higher mRNA and secreted levels of interferon b (IFNb), CXCL1, CXCL8/IL-8, CXCL9, and CXCL10 than cells treated with either ATRA or polyI:C. Silencing of MDA5 by siRNA moderately affected IFNb secretion, whereas TLR3 knockdown interfered with both CXCL chemokine and IFNb production. Furthermore, the supernatants of ATRA + polyI:C-activated cultures increased the migration of both human monocyte-derived macrophages and CD1a + dendritic cells significantly as compared with the supernatants of cells treated with either ATRA or polyI:C, and this effect occurred in a TLR3-dependent manner. In conclusion, consecutive treatment with ATRA and polyI:C results in strong, TLR3/MDA5-mediated chemokine and IFN responses in cultured human melanoma cells, which triggers a functional migratory response in professional antigen-presenting cells. This novel mode of concomitant activation may represent a more efficient treatment option for future melanoma therapy.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina
Megjelenés:	Melanoma Research 22 : 5 (2012), p. 351-361. -
További szerzők:	Osman, Rolah M. Bacskai Ildikó (1985-) (immunológus) Kumar, Brahma V. Agod Zsófia Lányi Árpád (1962-) (biológus, immunológus) Gogolák Péter (1968-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban NK101538 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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