A focused Real Time PCR strategy to determine GILZ expression in mouse tissues

Cari, Luigi; Ricci, E; Gentili, M; Petrillo, Maria Grazia; Ayroldi, Emira; Nocentini, Giuseppe; Riccardi, Carlo

doi:10.1016/j.rinim.2015.10.003

Cited by 14 publications

(12 citation statements)

References 28 publications

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“…We found that both in vitro and in vivo GILZ expression was enhanced as early as 3 h after GC (DEX) treatment. Up‐regulation of GILZ by DEX was previously also reported in circulating neutrophils in humans and correlated with apoptosis (16); thus, it seems that neutrophils are another myeloid cell type in which GILZ plays an important role (15, 30, 35).…”

Section: Discussionmentioning

confidence: 69%

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Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

et al. 2017

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The glucocorticoid-induced leucine zipper (GILZ) gene is a pivotal mediator of the anti-inflammatory effects of glucocorticoids (GCs) that are known to regulate the function of both adaptive and innate immunity cells. Our aim was to investigate the role of GILZ in GC-induced inhibition of neutrophil migration, as this role has not been investigated before. We found that GILZ expression was induced by dexamethasone (DEX), a synthetic GC, in neutrophils, and that it regulated migration of these cells into inflamed tissues under DEX treatment. Of note, inhibition of neutrophil migration was not observed in GILZ-knockout mice with peritonitis that were treated by DEX. This was because DEX was unable to up-regulate annexin A1 (Anxa1) expression in the absence of GILZ. Furthermore, we showed that GILZ mediates Anxa1 induction by GCs by transactivating Anxa1 expression at the promoter level via binding with the transcription factor, PU.1. The present findings shed light on the role of GILZ in the mechanism of induction of Anxa1 by GCs. As Anxa1 is an important protein for the resolution of inflammatory response, GILZ may represent a new pharmacologic target for treatment of inflammatory

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Section: Discussionmentioning

confidence: 69%

“…All reagents were purchased from Thermo Fisher Scientific (Waltham, MA, USA). GILZ was amplified as previously described with β‐actin as internal control (30). All experiments were carried out in triplicate, and the ∆∆ C t method was used to determine the expression of target genes.…”

Section: Methodsmentioning

confidence: 99%

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

et al. 2017

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“…For example, TSC22D3 or GILZ is one of the most upregulated genes in the microarray dataset that have been previously reported to inhibit migration of leukocytes (33). GILZ gene expression has been shown to be induced by dexamethasone in the whole eye of a mouse (34), and in cultured primary human lens epithelial cells (35), but its expression or its role in the cornea has not been explored. Tumor necrosis factor receptor superfamily, member 11b ( TNFRSF11b ), a promoter of migration (36), is one of the most-repressed genes in this microarray dataset, which was reported to be expressed in corneal stroma (37), however its regulation by glucocorticoids in the cornea has never been reported.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid action in human corneal epithelial cells establishes roles for corticosteroids in wound healing and barrier function of the eye

Kadmiel

Jànoshàzi

et al. 2016

Experimental Eye Research

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Glucocorticoids play diverse roles in almost all physiological systems of the body, including both anti-inflammatory and immunosuppressive roles. Synthetic glucocorticoids are one of the most widely prescribed drugs and are used in the treatment of conditions such as autoimmune diseases, allergies, ocular disorders and certain types of cancers. In the interest of investigating glucocorticoid actions in the cornea of the eye, we established that multiple cell types in mouse corneas express functional glucocorticoid receptor (GR) with corneal epithelial cells having robust expression. To define glucocorticoid actions in a cell type-specific manner, we employed immortalized human corneal epithelial (HCE) cell line to define the glucocorticoid transcriptome and elucidated its functions in corneal epithelial cells. Over 4000 genes were significantly regulated within 6 hours of dexamethasone treatment, and genes associated with cell movement, cytoskeletal remodeling and permeability were highly regulated. Real-time in vitro wound healing assays revealed that glucocorticoids delay wound healing by attenuating cell migration. These functional alterations were associated with cytoskeletal remodeling at the wounded edge of a scratch-wounded monolayer. However, glucocorticoid treatment improved the organization of tight-junction proteins and enhanced the epithelial barrier function. Our results demonstrate that glucocorticoids profoundly alter corneal epithelial gene expression and many of these changes likely impact both wound healing and epithelial cell barrier function.

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“…Glucocorticoid-induced leucine zipper is encoded by the TGF-β-stimulated clone (TSC) 22 domain family protein 3 ( Tsc22d3 ) gene located on the X-chromosome and is constitutively expressed in most tissues ( 12 , 16 , 28 ). GILZ is among the earliest and highest GC-induced genes.…”

Section: Gilz’s General Propertiesmentioning

confidence: 99%

Glucocorticoid-Induced Leucine Zipper: Fine-Tuning of Dendritic Cells Function

Vétillard

Schlecht-Louf

2018

Front. Immunol.

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Dendritic cells (DCs) are key antigen-presenting cells that control the induction of both tolerance and immunity. Understanding the molecular mechanisms regulating DCs commitment toward a regulatory- or effector-inducing profile is critical for better designing prophylactic and therapeutic approaches. Initially identified in dexamethasone-treated thymocytes, the glucocorticoid-induced leucine zipper (GILZ) protein has emerged as a critical factor mediating most, but not all, glucocorticoids effects in both non-immune and immune cells. This intracellular protein exerts pleiotropic effects through interactions with transcription factors and signaling proteins, thus modulating signal transduction and gene expression. GILZ has been reported to control the proliferation, survival, and differentiation of lymphocytes, while its expression confers anti-inflammatory phenotype to monocytes and macrophages. In the past twelve years, a growing set of data has also established that GILZ expression in DCs is a molecular switch controlling their T-cell-priming capacity. Here, after a brief presentation of GILZ isoforms and functions, we summarize current knowledge regarding GILZ expression and regulation in DCs, in both health and disease. We further present the functional consequences of GILZ expression on DCs capacity to prime effector or regulatory T-cell responses and highlight recent findings pointing to a broader role of GILZ in the fine tuning of antigen capture, processing, and presentation by DCs. Finally, we discuss future prospects regarding the possible roles for GILZ in the control of DCs function in the steady state and in the context of infections and chronic pathologies.

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A focused Real Time PCR strategy to determine GILZ expression in mouse tissues

Cited by 14 publications

References 28 publications

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

Role of the glucocorticoid‐induced leucine zipper gene in dexamethasone‐induced inhibition of mouse neutrophil migration via control of annexin A1 expression

Glucocorticoid action in human corneal epithelial cells establishes roles for corticosteroids in wound healing and barrier function of the eye

Glucocorticoid-Induced Leucine Zipper: Fine-Tuning of Dendritic Cells Function

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