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001-es BibID:BIBFORM057163
Első szerző:Garabuczi Éva (biokémikus, molekuláris biológus)
Cím:Glucocorticoids enhance prolonged clearance of apoptotic cells by upregulating liver X receptor, peroxisome proliferator-activated receptor-[delta] and UCP2 / Éva Garabuczi, Zsolt Sarang, Zsuzsa Szondy
Dátum:2014
ISSN:0006-3002
Megjegyzések:Efficient phagocytic clearance of apoptotic cells (efferocytosis) is essential to prevent the development of chronic inflammation and autoimmunity. Glucocorticoids are widely used in the therapy of chronic inflammatory diseases, and increasing evidence suggests that they act partly via enhancing efferocytosis by macrophages. Glucocorticoids were previously shown to promote both protein S- and MFG-E8-dependent efferocytosis. Since previous studies in our laboratory have demonstrated that glucocorticoids induce the expression of retinaldehyde dehydrogenases in macrophages, in the present experiments the possible involvement of retinoids in the glucocorticoid-induced efferocytosis was studied in mouse bone marrow derived macrophages. Here we show that glucocorticoids promote not only short-term, but also long-term clearance of apoptotic cells. Glucocorticoids seem to directly induce the expression of the phagocytosis-related genes MERTK, C1q, UCP2, and the transcription factor C/EBPβ. C/EBPβ contributes to the further induction of the phagocytosis-related genes, and is required for the induction of lipid sensing receptors LXRs, PPAR?, RARα, RXRα and RALDH1, the latter one in an LXR- and RARα-dependent manner. Glucocorticoid-induced enhancement in long-term efferocytosis was dependent on the induction of lipid sensing receptors known to be triggered by the lipid content of the engulfed cells to enhance phagocytic capacity. Retinoids did not affect the glucocorticoid-induced short term phagocytosis of apoptotic cells, but were required for the glucocorticoid-induced enhancement of efferocytosis during prolonged clearance of apoptotic cells by promoting efficient LXR and PPAR? upregulation. Our data indicate that retinoids could be considered as potential promoters of the efficacy of glucocorticoid treatment in inflammatory diseases.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Efferocytosis
Glucocorticoid
LXR
Macrophage
PPAR?
UCP2
Megjelenés:Biochimica et Biophysica Acta (BBA). Molecular Cell Research. - 1853 : 3 (2014), p. 573-582. -
További szerzők:Sarang Zsolt (1976-) (mikrobiológus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
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2.

001-es BibID:BIBFORM057165
Első szerző:Kiss Beáta (biokémikus, molekuláris biológus)
Cím:Retinoids induce Nur77-dependent apoptosis in mouse thymocytes / Beáta Kiss, Katalin Tóth, Zsolt Sarang, Éva Garabuczi, Zsuzsa Szondy
Dátum:2015
ISSN:0167-4889
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 retinoic acids induce the expression of Nur77, and retinoid-induced apoptosis is completely dependent on Nur77, as retinoids were unable to induce apoptosis in Nur77 null thymocytes. In wild-type thymocytes retinoids induced enhanced expression of the 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 Nur77-dependent induction of STAT1 leading to enhanced Bim expression, and 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 STAT1. Our data together indicate that retinoids induce a Nur77-dependent cell death program in thymocytes activating the mitochondrial pathway of apoptosis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis
Nur77
Retinoid
Thymocyte
PPAR
UCP2
Megjelenés:Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. - 1853 : 3 (2015), p. 660-670. -
További szerzők:Tóth Katalin Ágnes (1977-) (biokémikus, molekuláris biológus) Sarang Zsolt (1976-) (mikrobiológus) Garabuczi Éva (1982-) (biokémikus, molekuláris biológus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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