Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice.

@article{Delfino2004DecreaseOB,
  title={Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice.},
  author={Domenico Vittorio Delfino and Massimiliano Agostini and Stefania Spinicelli and Pasquale Vito and Carlo Riccardi},
  journal={Blood},
  year={2004},
  volume={104 13},
  pages={
          4134-41
        }
}
Glucocorticoids promote thymocyte apoptosis and modulate transcription of numerous genes. GILZ (glucocorticoid-induced leucine zipper), being one of them, is strongly up-regulated in the thymus. To elucidate its function we generated transgenic mice overexpressing it specifically in the T-cell lineage and characterized its influence on thymus function. In young adult transgenic mice CD4(+)CD8(+) thymocyte number was significantly decreased and ex vivo thymocyte apoptosis was increased… Expand
Bcl-xL overexpression decreases GILZ levels and inhibits glucocorticoid-induced activation of caspase-8 and caspase-3 in mouse thymocytes
TLDR
The presence of a glucocorticoid-induced apoptosis self-amplification loop in which GILZ decreases Bcl-xL expression with a subsequent activation of caspase-8 and caspases-3 is suggested, which enhances the stability and accumulation of GilZ and ensures the unimpeded and irreversible progression of apoptosis. Expand
Inhibited cell death, NF-kappaB activity and increased IL-10 in TCR-triggered thymocytes of transgenic mice overexpressing the glucocorticoid-induced protein GILZ.
TLDR
The hypothesis that GILZ regulates, at least in part, T-cell development by influencing thymus function at cellular and molecular levels is supported. Expand
Increased GILZ expression in transgenic mice up-regulates Th-2 lymphokines.
TLDR
It is demonstrated that Gilz contributes to CD4+ commitment toward a Th-2 phenotype and suggested this contribution may be another mechanism accounting for glucocorticoid immunomodulation. Expand
Glucocorticoid-Induced Leucine Zipper Is Expressed in Human Neutrophils and Promotes Apoptosis through Mcl-1 Down-Regulation
TLDR
Results reveal GILZ to be a new actor in apoptosis regulation in neutrophil-like cells involving JNK and Mcl-1, suggesting that GILz-induced apoptosis used the mitochondrial pathway. Expand
Lack of glucocorticoid-induced leucine zipper (GILZ) deregulates B-cell survival and results in B-cell lymphocytosis in mice.
TLDR
It is shown that deletion of GILZ in mice leads to an accumulation of B lymphocytes in the bone marrow, blood, and lymphoid tissues, and suggested that the deregulation of GilZ expression could be implicated in the pathogenesis of B-cell disorders. Expand
Glucocorticoids Repress bcl-X Expression in Lymphoid Cells by Recruiting STAT5B to the P4 Promoter*
TLDR
It is shown that, on mouse thymocytes and T lymphocyte derivative S49 cells, glucocorticoids inhibited transcription from P4 and decreased the ratio bcl-XL/bcl-XS favoring apoptosis, which is similar to that of antiapoptotic cells. Expand
GILZ overexpression attenuates endoplasmic reticulum stress-mediated cell death via the activation of mitochondrial oxidative phosphorylation.
TLDR
A new role of GILZ is revealed, which acts as a cytoprotector against ER stress through a pathway involving mitochondrial OXPHOS, which is abolished in cells depleted of mitochondrial DNA, which are OX PHOS-deficient. Expand
Role of caspase-8 in thymus function
The thymus is the primary organ responsible for de novo generation of immunocompetent T cells that have a diverse repertoire of antigen recognition. During the developmental process, 98% ofExpand
Glucocorticoid induced leucine zipper inhibits apoptosis of cardiomyocytes by doxorubicin.
TLDR
The data suggest that GILZ functions as a cytoprotective gene in cardiomyocytes, and glucocorticoid-induced leucine zipper (GILZ) to be a mediator of GC-induced cy toprotection. Expand
Genomic and non-genomic effects of different glucocorticoids on mouse thymocyte apoptosis.
TLDR
Different glucocorticoids have different apoptotic activity which is related to their ability to induce both genomic effects, evaluation as caspases activation and GILZ expression, and non-genomic effects, evaluated as PI-PLC phosphorylation. Expand
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