Találati lista | Tudóstér

001-es BibID:	BIBFORM043609
Első szerző:	Albert Réka
Cím:	Cultivation and characterization of cornea limbal epithelial stem cells on lens capsule in animal material-free medium / Réka Albert, Zoltán Veréb, Krisztián Csomós, Morten C. Moe, Erik O. Johnsen, Ole Kristoffer Olstad, Bjørn Nicolaissen, Éva Rajnavölgyi, László Fésüs, András Berta, Goran Petrovski
Dátum:	2012
ISSN:	1932-6203
Megjegyzések:	A simple, reproducible, animal-material free method for cultivating and characterizing cornea limbal epithelial stem cells (LESCs) on human lens capsule (LC) was developed for future clinical transplantation. The limbal tissue explants (2 ? 2 ? 0.25 mm) were harvested from 77 cadavers and expanded ex vivo on either cell culture plates or LC in medium containing human serum as the only growth supplement. Cell outgrowth at the edge of the explants was observed within 24 hours of cultivation and achieved viable outgrowth (>97% viability as measured by MTT assay and flow cytometry) within two weeks. The outgrowing cells were examined by genome-wide microarray including markers of stemness (p63?, ABCG2, CK19, Vimentin and Integrin ?9), proliferation (Ki-67), limbal epithelial cells (CK 8/18 and 14) and differentiated cornea epithelial cells (CK 3 and 12). Immunostaining revealed the non-hematopoietic, -endothelial and -mesenchymal stem cell phenotype of the LESCs and the localization of specific markers in situ. Cell adhesion molecules, integrins and lectin-based surface carbohydrate profiling showed a specific pattern on these cells, while colony-formation assay confirmed their clonal potency. The LESCs expressed a specific surface marker fingerprint (CD117/c-kit, CXCR4, CD144/VE-Cadherin, CD146/MCAM, CD166/ALCAM, and surface carbohydrates: WGA, ConA, RCA, PNA and AIL) which can be used for better localization of the limbal stem cell niche. In summary, we report a novel method combining the use of a medium with human serum as the only growth supplement with LC for cultivating, characterizing and expanding cornea LESCs from cadavers or alternatively from autologous donors for possible treatment of LESC deficiency.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Limbal epithelial stem cell egyetemen (Magyarországon) készült közlemény
Megjelenés:	PLoS One. - 7 : 10 (2012), p. e47187. -
További szerzők:	Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Csomós Krisztián (1981-) (molekuláris biológus) Moe, Morten C. Johnsen, Erik O. Olstad, Ole Kristoffer Nicolaissen, Bjorn Rajnavölgyi Éva (1950-) (immunológus) Fésüs László (1947-) (orvos biokémikus) Berta András (1955-) (szemész, gyermekszemész) Petrovski, Goran (1975-) (orvos)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM035234
Első szerző:	Ayna, Gizem (biotechnológus)
Cím:	ATP release from dying autophagic cells and their phagocytosis are crucial for inflammasome activation in macrophages / Gizem Ayna, Dmitri V. Krysko, Agnieszka Kaczmarek, Goran Petrovski, Peter Vandenabeele, László Fésüs
Dátum:	2012
ISSN:	1932-6203
Megjegyzések:	Pathogen-activated and damage-associated molecular patterns activate the inflammasome in macrophages. We report that mouse macrophages release IL-1? while co-incubated with pro-B (Ba/F3) cells dying, as a result of IL-3 withdrawal, by apoptosis with autophagy, but not when they are co-incubated with living, apoptotic, necrotic or necrostatin-1 treated cells.NALP3-deficient macrophages display reduced IL-1? secretion, which is also inhibited inmacrophages deficient in caspase-1 or pre-treated with its inhibitor. This finding demonstrates that the inflammasome is activated during phagocytosis of dying autophagic cells. We show that activation of NALP3 depends on phagocytosis of dying cells, ATP release through pannexin-1 channels of dying autophagic cells, P2X7 purinergic receptor ctivation, and on consequent potassium efflux. Dying autophagic Ba/F3 cells injected intraperitoneally in micerecruit neutrophils and thereby induce acute inflammation. These findings demonstrate that NALP3 performs key upstream functions in inflammasome activation in mouse macrophagesengulfing dying autophagic cells, and that these functions lead to pro-inflammatory responses.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban autophagy apoptosis phagocytosis by macrophages NALP3 pannexin-1 channel külföldön készült közlemény
Megjelenés:	Plos One. - 7 : 6 (2012), p. e40069. -
További szerzők:	Krysko, Dmitri V. Kaczmarek, Agnieszka Petrovski, Goran (1975-) (orvos) Vandenabeele, Peter Fésüs László (1947-) (orvos biokémikus)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM069234
035-os BibID:	(cikkazonosító)e0172189 (WOS)000395983500029 (Scopus)85014323809
Első szerző:	Thangaraju, Kiruphagaran
Cím:	Genomic variants reveal differential evolutionary constraints on human transglutaminases and point towards unrecognized significance of transglutaminase 2 / Thangaraju Kiruphagaran, Király Róbert, Demény Máté A., Mótyán János András, Fuxreiter Mónika, Fésüs László
Dátum:	2017
ISSN:	1932-6203
Megjegyzések:	Transglutaminases (TGMs) catalyze Ca2+-dependent transamidation of proteins with specified roles in blood clotting (F13a) and in cornification (TGM1, TGM3). The ubiquitous TGM2 has well described enzymatic and non-enzymatic functions but in-spite of numerous studies its physiological function in humans has not been defined. We compared data on non-synonymous single nucleotide variations (nsSNVs) and loss-of-function variants on TGM1-7 and F13a from the Exome aggregation consortium dataset, and used computational and biochemical analysis to reveal the roles of damaging nsSNVs of TGM2. TGM2 and F13a display rarer damaging nsSNV sites than other TGMs and sequence of TGM2, F13a and TGM1 are evolutionary constrained. TGM2 nsSNVs are predicted to destabilize protein structure, influence Ca2+ and GTP regulation, and non-enzymatic interactions, but none coincide with conserved functional sites. We have experimentally characterized six TGM2 allelic variants detected so far in homozygous form, out of which only one, p.Arg222Gln, has decreased activities. Published exome sequencing data from various populations have not uncovered individuals with homozygous loss-of-function variants for TGM2, TGM3 and TGM7. Thus it can be concluded that human transglutaminases differ in harboring damaging variants and TGM2 is under purifying selection suggesting that it may have so far not revealed physiological functions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Plos One. - 12 : 3 (2017), p. 1-24. -
További szerzők:	Király Róbert (1975-) (biológus) Demény Máté Ágoston (1976-) (molekuláris biológus) Mótyán János András (1981-) (biokémikus, molekuláris biológus) Fuxreiter Mónika (1969-) (kutató vegyész) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:	NK-105046 OTKA NN-106562 OTKA TÁMOP-4.2.2.A-11/1/KONV-2012-0023 TÁMOP MTA-LP2012-41 Egyéb RH/885/2013 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM028038
Első szerző:	Zahuczky Gábor (molekuláris biológus, biokémikus, vegyész)
Cím:	Differentiation and Glucocorticoid Regulated Apopto-Phagocytic Gene Expression Patterns in Human Macrophages : role of Mertk in Enhanced Phagocytosis / Gábor Zahuczky, Endre Kristóf, Gyöngyike Majai, László Fésüs
Dátum:	2011
Megjegyzések:	The daily clearance of physiologically dying cells is performed safely mainly by cells in the mononuclear phagocyte system. They can recognize and engulf dying cells utilizing several cooperative mechanisms. In our study we show that the expression of a broad range of apopto-phagocytic genes is strongly up-regulated during differentiation of human monocytes to macrophages with different donor variability. The glucocorticoid dexamethasone has a profound effect on this process by selectively up-regulating six genes and down-regulating several others. The key role of the up-regulated mer tyrosine kinase (Mertk) in dexamethasone induced enhancement of phagocytosis could be demonstrated in human monocyte derived macrophages by gene silencing as well as blocking antibodies, and also in a monocyte-macrophage like cell line. However, the additional role of other glucocorticoid induced elements must be also considered since the presence of autologous serum during phagocytosis could almost completely compensate for the blocked function of Mertk.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina
Megjelenés:	PLoS ONE. - 6 : 6 (2011), p. e21349. -
További szerzők:	Kristóf Endre (1987-) (általános orvos) Majai Gyöngyike (1977-) (belgyógyász, immunológus) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Az apoptózis molekuláris mechanizmusa NI 67877 OTKA MRTNCT-2006-036032 EGYÉB MRTN-CT 2006-035624 EGYÉB LSHB-CT-2007-037730 EGYÉB
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
Borító:
Saját polcon: