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001-es BibID:	BIBFORM028770
Első szerző:	Szegezdi Éva
Cím:	Apoptosis-linked in vivo regulation of the tissue transglutaminase gene promoter / É. Szegezdi, Zs. Szondy, L. Nagy, Z. Nemes, R. R. Friis, P. J. A. Davies, L. Fésüs
Dátum:	2000
ISSN:	1350-9047
Megjegyzések:	Tissue transglutaminase (tTG) is upregulated in various cells undergoing apoptosis. To investigate the transcriptional regulation of tTG a mouse strain carrying a beta-galactosidase reporter gene under the control of a 3.8 kilobase fragment of the tTG promoter was characterised. The transgene construct was shown to be expressed in the apoptotic regions of the mouse embryo. Here we report that the regulation of the transgene is also apoptosis-linked in adult animals. The transgene is induced in endocrine apoptosis involving mammary gland involution and corpus luteum regression. Induction of the reporter gene is detectable during in vivo but not in vitro apoptosis of thymocytes induced by the glucocorticoid receptor, the nur77, p53 and the retinoid receptor gamma mediated pathways. Additionally, the lacZ expression mimics the activation of the endogenous promoter in tissues characterised by high apoptotic turnover. These results suggest that the apoptosis-specific transcriptional regulation of tTG is mediated through elements of a 3.8 kb promoter and may require cosignals available only in tissue environment.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk egyetemen (Magyarországon) készült közlemény
Megjelenés:	Cell Death and Differentiation. - 7 : 12 (2000), p. 1225-1233. -
További szerzők:	Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Nemes Zoltán (1942-) (patológus) Friis, Bob R. R. Davies, Peter J. A. Fésüs László (1947-) (orvos biokémikus)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM033821
035-os BibID:	(WoS)000300876300003 (Scopus)84857734407
Első szerző:	Tsakiris, Ioannis (orvos)
Cím:	Carboxypeptidase-M is regulated by lipids and CSFs in macrophages and dendritic cells and expressed selectively in tissue granulomas and foam cells / Tsakiris I., Torocsik D., Gyongyosi A., Dozsa A., Szatmari I., Szanto A., Soos G., Nemes Z., Igali L., Marton I., Takats Z., Nagy L., Dezso B.
Dátum:	2012
ISSN:	0023-6837
Megjegyzések:	Granulomatous inflammations, characterized by the presence of activated macrophages (MAs) forming epithelioid cell (EPC) clusters, are usually easy to recognize. However, in ambiguous cases the use of a MA marker that expresses selectively in EPCs may be needed. Here, we report that carboxypeptidase-M (CPM), a MA-differentiation marker, is preferentially induced in EPCs of all granuloma types studied, but not in resting MAs. As CPM is not expressed constitutively in MAs, this allows utilization of CPM-immunohistochemistry in diagnostics of minute granuloma detection when dense non-granulomatous MAs are also present. Despite this rule, hardly any detectable CPM was found in advanced/active tubercle caseous disease, albeit in early tuberculosis granuloma, MAs still expressed CPM. Indeed, in vitro both the CPM-protein and -mRNA became downregulated when MAs were infected with live mycobacteria. In vitro, MA-CPM transcript is neither induced remarkably by interferon-γ, known to cause classical MA activation, nor by IL-4, an alternative MA activator. Instead, CPM is selectively expressed in lipid-laden MAs, including the foam cells of atherosclerotic plaques, xanthomatous lesions and lipid pneumonias. By using serum, rich in lipids, and low-density lipoprotein (LDL) or VLDL, CPM upregulation could be reproduced in vitro in monocyte-derived MAs both at transcriptional and protein levels, and the increase is repressed under lipid-depleted conditions. The microarray analyses support the notion that CPM induction correlates with a robust progressive increase in CPM gene expression during monocyte to MA maturation and dendritic cell (DC) differentiation mediated by granulocyte-MA-colony-stimulating factor+IL-4. M-CSF alone also induced CPM. These results collectively indicate that CPM upregulation in MAs is preferentially associated with increased lipid uptake, and exposure to CSF, features of EPCs, also. Therefore, CPM-immunohistochemistry is useful for granuloma and foam MA detections in tissue sections. Furthermore, the present data offer CPM for the first time to be a novel marker and cellular player in lipid uptake and/or metabolism of MAs by promoting foam cell formation.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk open access article
Megjelenés:	Laboratory Investigation. - 92 : 3 (2012), p. 345-361. -
További szerzők:	Töröcsik Dániel (1979-) (bőrgyógyász) Gyöngyösi Adrienn (1982-) (biológus) Dózsa Anikó (1978-) (Ph.D hallgató, orvos) Szatmári István (1971-) (biológus) Szántó Attila (1976-) (orvos, biokémikus) Soós Györgyike (1959-) (pathológus) Nemes Zoltán (1942-) (patológus) Igali László Márton Ildikó (1954-) (fogszakorvos) Takáts Zoltán Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Dezső Balázs (1951-) (pathológus)
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