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001-es BibID:	BIBFORM037170
Első szerző:	Garabuczi Éva (biokémikus, molekuláris biológus)
Cím:	Retinoids produced by macrophages engulfing apoptotic cells contribute to the appearance of transglutaminase 2 in apoptotic thymocytes / Éva Garabuczi, Beáta Kiss, Szabolcs Felszeghy, Gregory J. Tsay, László Fésüs, Zsuzsa Szondy
Dátum:	2012
Megjegyzések:	Transglutaminase 2 (TG2) has been known for a long time to be associated with the in vivo apoptosis program of various cell types including T cells. Though the expression of the enzyme was strongly induced in mouse thymocytes following apoptosis induction in vivo, no significant induction of TG2 could be detected, when thymocytes were induced to die by the same stimuli in vitro indicating that signals arriving from the tissue environment are required for the in vivo induction of the enzyme in apoptotic thymocytes. Previous studies have shown that one of these signals is TGF-beta which is released by macrophages engulfing apoptotic cells. Besides TGF-beta the TG2 promoter contains retinoic acid response elements as well. Here we show that in vitro retinoic acids, or TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes, and the apoptotic signal contributes to the TG2 induction. Inhibition of retinoic acid synthesis either by aldehyde or retinaldehyde dehydrogenases significantly attenuates the in vivo induction of TG2 following apoptosis induction indicating that retinoids indeed might contribute in vivo to the apoptosis-related TG2 expression. What is more, the in vivo apoptosis induction in the thymus is accompanied by an enhanced retinoid dependent transcriptional activity possibly due to the enhanced retinoid synthesis by macrophages engulfing apoptotic cells. Our data reveal a new crosstalk between macrophages and apoptotic cells, in which apoptotic cell uptake-induced retinoid synthesis in macrophages enhances TG2 expression in the dying thymocytes.
ISBN:	978-953-95551-4-4
Tárgyszavak:	Természettudományok Biológiai tudományok előadáskivonat TG2 thymocyte retinoids macrophage
Megjelenés:	FEBS3 + Meeting From molecules to life and back, Book of abstracts / eds. Jerka Dumic, Zrinka Kovarik, Jadranka Varljen. - p. 203. -
További szerzők:	Kiss Beáta (1984-) (biokémikus, molekuláris biológus) Felszeghy Szabolcs Béla (1972-) (fogorvos, anatómus, kötőszövetbiológus) Tsay, Gregory J. Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Pályázati támogatás:	TÁMOP-4.2.2/B-10/1-2010-0024 TÁMOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM028039
Első szerző:	Garabuczi Éva (biokémikus, molekuláris biológus)
Cím:	Retinoids produced by macrophages engulfing apoptotic cells contribute to the appearance of transglutaminase 2 in apoptotic thymocytes / Garabuczi Éva, Kiss Beáta, Felszeghy Szabolcs, Tsay Gregory J., Fésüs László, Szondy Zsuzsa
Dátum:	2013
ISSN:	0939-4451
Megjegyzések:	Transglutaminase 2 (TG2) has been known for a long time to be associated with the in vivo apoptosis program of various cell types including T cells. Though the expression of the enzyme was strongly induced in mouse thymocytes following apoptosis induction in vivo, no significant induction of TG2 could be detected, when thymocytes were induced to die by the same stimuli in vitro indicating that signals arriving from the tissue environment are required for the in vivo induction of the enzyme in apoptotic thymocytes. Previous studies have shown that one of these signals is transforming growth factor-β (TGF-β) which is released by macrophages engulfing apoptotic cells. Besides TGF-β, the TG2 promoter contains retinoic acid response elements as well. Here we show that in vitro retinoic acids, or TGF-β and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes, and the apoptotic signal contributes to the TG2 induction. Inhibition of retinoic acid synthesis either by alcohol or retinaldehyde dehydrogenases significantly attenuates the in vivo induction of TG2 following apoptosis induction indicating that retinoids indeed might contribute in vivo to the apoptosis-related TG2 expression. What is more, the in vivo apoptosis induction in the thymus is accompanied by an enhanced retinoid-dependent transcriptional activity due to the enhanced retinoid synthesis by macrophages engulfing apoptotic cells. Our data reveal a new crosstalk between macrophages and apoptotic cells, in which apoptotic cell uptake-induced retinoid synthesis in macrophages enhances TG2 expression in the dying thymocytes.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina egyetemen (Magyarországon) készült közlemény
Megjelenés:	Amino Acids. - 44 : 1 (2013), p. 235-244. -
További szerzők:	Kiss Beáta (1984-) (biokémikus, molekuláris biológus) Felszeghy Szabolcs Béla (1972-) (fogorvos, anatómus, kötőszövetbiológus) Tsay, Gregory J. Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Az apoptózis és a fagocitózis folyamatának összehangolása a szövetet tönkretevő gyulladási reakciók elkerülésére TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Az apoptózis molekuláris mechanizmusa
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001-es BibID:	BIBFORM037168
Első szerző:	Kiss Beáta (biokémikus, molekuláris biológus)
Cím:	Retinoids Induce A Nur77-Dependent Apoptosis In Mouse Thymocytes / Beata Kiss, Katalin Tóth, Zsolt Sarang, Éva Garabuczi, László Fésüs, Zsuzsa Szondy
Dátum:	2012
Megjegyzések:	Nur77 is a transcription factor, which plays a determinant role in mediating T cell receptor-induced cell death of thymocytes. In addition to regulation of transcription, Nur77 contributes to apoptosis induction by targeting mitochondria, where it can convert Bcl-2, an anti-apoptotic protein into a proapoptotic molecule. Previous studies have demonstrated that retinoids are actively produced in the mouse thymus and can induce a transcription-dependent apoptosis in mouse thymocytes. Here we show that similar to TCR stimulation, retinoic acids also induce the expression of Nur77 in a dose-dependent manner, 9-cis retinoic acid being more effective than all-trans retinoic acid. Retinoid-induced apoptosis was found to be completely dependent on Nur77, as retinoids were unable to induce apoptosis in Nur77 null thymocytes. In wild-type thymocytes retinoids induced the expression of five apoptosis-related genes, FasL, TRAIL, NDG-1, Gpr65 and Bid, all of them in a Nur77-dependent manner. The combined action of these proteins led to Caspase 8-dependent Bid cleavage in the mitochondria. In addition, we could demonstrate the mitochondrial translocation of Nur77 leading to the exposure of the Bcl-2/BH3 domain. The retinoid-induced apoptosis was dependent on both Caspase 8 and 9. Our data together indicate that retinoids induce a Nur77-dependent cell death program in thymocytes activating the mitochondrial pathway of apoptosis.
ISBN:	978-953-95551-4-4
Tárgyszavak:	Természettudományok Biológiai tudományok előadáskivonat Retinoids Nur77
Megjelenés:	FEBS3 + Meeting From molecules to life and back, Book of abstracts / eds. Jerka Dumic, Zrinka Kovarik, Jadranka Varljen. - p. 111. -
További szerzők:	Tóth Katalin Ágnes (1977-) (biokémikus, molekuláris biológus) Sarang Zsolt (1976-) (mikrobiológus) Garabuczi Éva (1982-) (biokémikus, molekuláris biológus) Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Pályázati támogatás:	TÁMOP-4.2.2/B-10/1-2010-0024 TÁMOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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