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PHK Cells: control vs. cyclosporine vs. 11R-VIVIT

ABSTRACT: Calcineurin/NFAT signaling pathway has been shown to play important roles in various tissues such as the immune system, cardiac muscle and neuron. Although recent studies have shown that the pathway is involved in the regulation of hair growth, the precise mechanism is still unclear. In this study, we examine the molecular mechanism which is regulated by calcineurin/NFAT pathway, using two specific inhibitors for the pathway. Transcriptional profiling of human keratinocyte cell line, PHK cells, comparing control untreated PHK cells with cyclosporin A (CsA)-treated or 11R-VIVIT-treated PHK cells. Goal was to identify the effects of NFAT inhibitors on PHK cell proliferation. Cyclosporine A is a chemical compound, which strongly inhibits calcineurin phosphatase activity cooperating with cyclophilin, resulting in inhibition of NFAT signaling pathway. 11R-VIVIT is a cell-permeable peptide, which specifically interacts with NFAT and inhibits its binding to calcineurin, resulting in competitive inhibition of NFAT signaling pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25175 | GEO | 2010/11/08

SECONDARY ACCESSION(S): PRJNA134435

REPOSITORIES: GEO

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PHK Cells: control vs. cyclosporine vs. 11R-VIVIT

Project description:Calcineurin/NFAT signaling pathway has been shown to play important roles in various tissues such as the immune system, cardiac muscle and neuron. Although recent studies have shown that the pathway is involved in the regulation of hair growth, the precise mechanism is still unclear. In this study, we examine the molecular mechanism which is regulated by calcineurin/NFAT pathway, using two specific inhibitors for the pathway. Transcriptional profiling of human keratinocyte cell line, PHK cells, comparing control untreated PHK cells with cyclosporin A (CsA)-treated or 11R-VIVIT-treated PHK cells. Goal was to identify the effects of NFAT inhibitors on PHK cell proliferation. Cyclosporine A is a chemical compound, which strongly inhibits calcineurin phosphatase activity cooperating with cyclophilin, resulting in inhibition of NFAT signaling pathway. 11R-VIVIT is a cell-permeable peptide, which specifically interacts with NFAT and inhibits its binding to calcineurin, resulting in competitive inhibition of NFAT signaling pathway. Three-condition experiment; untreated PHK cells, CsA-treated PHK cells and 11R-VIVIT-treated PHK cells. Supplementary files: Significantly up-regulated genes across 4 different comparisons.

2010-11-08 | E-GEOD-25175 | biostudies-arrayexpress

Calcineurin/NFAT signaling inhibits myeloid hematopoiesis in mice.

Project description:Nuclear factor of activated T cells (NFAT) comprises a family of transcription factors that regulate T cell development, activation and differentiation. NFAT signaling can also mediate granulocyte and DC activation, but it is unknown whether NFAT influences their development from progenitors. Here we report a novel role for calcineurin/NFAT signaling as a negative regulator of myeloid hematopoiesis. Reconstituting lethally-irradiated mice with hematopoietic stem cells expressing an NFAT-inhibitory peptide resulted in enhanced development of the myeloid compartment. Culturing bone marrow cells with Flt3-L and Cyclosporin A, which inhibits NFAT signaling, increased numbers of differentiated DC. Global gene expression analysis of untreated DC and NFAT-inhibited DC revealed differential expression of transcripts that regulate cell cycle and apoptosis. Thus, calcineurin/NFAT signaling negatively regulates myeloid lineage development. The finding that NFAT acts as a negative regulator of myeloid development provides novel insight in understanding immune responses during treatment with calcineurin/NFAT inhibitors as Cyclosporin A. bone marrow cells from C57B/6 mice were stimulated in Flt3-L suplemented media in presence or absence of calcineurin/NFAT inhibitor Cyclosporin A, samples in 3 biological replicates

2011-09-30 | E-GEOD-29094 | biostudies-arrayexpress

Granulocyte-monocyte progenitor cell cycle regulation occurs through calcium flux and calcineurin-NFAT signaling via Flt3-L

Project description:Complex regulatory mechanisms control continuous maintenance of myeloid progenitors and renewal of differentiated cells. Transcription factors play a important role in these processes. Here we report that the activation the calcineurin-NFAT signaling pathway inhibit the proliferation of myeloid granulocyte-monocyte progenitor (GMP). Myeloid progenitor subtypes possessed different susceptibilities to Ca2+ flux induction and consequently differential engagement of the calcineurin-NFAT pathway. This study show that inhibition of the calcineurin-NFAT pathway enhanced proliferation of GMPs both in vivo and in vitro. The calcineurin-NFAT signaling in GMPs is initiated through Flt3-L. The inhibition of the calcineurin-NFAT pathway altered the expression of the cell cycle regulation genes CDK4, CDK6, and CDKN1A, thus enabling faster cell cycle progression. The extensive use of NFAT inhibitors in the clinic should take into account that, in addition to the immunosuppression role in lymphoid cells, these NFAT inhibitors also affect the maintenance of the myeloid compartment. Microarray technology was used to understand the effects of NFAT inhibitors on C-kit enriched lineage negative cells.

2014-12-31 | GSE47208 | GEO

Calcineurin/NFAT signaling inhibits myeloid hematopoiesis in mice.

2011-10-01 | GSE29094 | GEO

Identification of differential expressed genes among reprogrammed cells cultured under control condition and calcineurin-NFAT pathway inhibition condition at reprogramming day 3 and day 6 through genome-wide transcript profiling

Project description:Inhibition of calcineurin-NFAT pathway at the early stage can block somatic cell reprogramming. In order to study how the calcineurin-NFAT pathway contributes to the early stage of reprogramming, we designed this microarray experiment and tried to find out which genes or signalings were changed after inhibition of calcineurin-NFAT signaling by CSA (a specific inhibitor of calcineurin-NFAT pathway).

2015-12-01 | GSE67739 | GEO

Mus musculus

Project description:Calcineurin/NFAT signaling inhibits myeloid hematopoiesis in mice.

| PRJNA140321 | ENA

Discovery of inhibitors of the HSP90-Calcineurin-NFAT pathway against glioblastoma

Project description:Discovery of inhibitors of the HSP90-Calcineurin-NFAT pathway against glioblastoma

| PRJNA428485 | ENA

Genome-wide analysis of gene expression regulated by calcineurin-NFAT signaling in mouse embryonic stem cells

Project description:Self-renewal and pluripotency are hallmarks of embryonic stem cells (ESCs). However, signaling pathways triggering their transition from self-renewal to differentiation are not well defined. Here, we report that the calcineurin-NFAT signaling pathway is both necessary and sufficient to switch ESCs from an undifferentiated state to early differentiation.To gain an insight into the function of calcinerin-NFAT signaling in ESC lineage commitment, we examined the repertoire of genes changed after LIF withdrawal alone, LIF withdrawal in the presence of cyclosporine A (CsA), a specific inhibitor of calcinerin and forced expression of active forms of calcineurin (deltaCnA) in the presence of LIF,and identified distinct classes of up and down regulated genes by calcineurin-NFAT signaling in mouse embryonic stem cells.

2011-01-01 | GSE21378 | GEO

Activating CD8 T cell clones via the T cell receptor complex in the absence and presence of cyclosporine A

Project description:Comparison of a cyclosporine-resistant murine CD8 T cell clone to a cyclosporine-sensitive murine T cell clone during activation (CSA = Cyclosporine A) Chronic allograft rejection is the leading cause of morbidity/mortality in solid organ and bone marrow transplant patients. It occurs in the setting of potent calcineurin and mTOR inhibitor therapies, implying that T cells mediating chronic rejection can function with compromised calcineurin-NFAT or IL-2 receptor signaling pathways. In murine models the T cells mediating allograft rejection in the setting of calcineurin inhibitor therapy are CD8 T cells making IFN-gamma without a requirement for perforin. It is not known whether these pathologic T cells are a unique subset or how they function. In parallel other animal model research has shown that alloepthelial cells residing in the donor organ are critical targets for rejection. While investigating T cell-alloepithelial cell interactions, we discovered an unusual alloreactive CD8 T cell population that recognized MHC class II I-Abm12. A CD8 T cell clone derived from that population was intrinsically-resistant to cyclosporine and rapamycin without prior exposure to either in vivo or in vitro. Microarray analysis comparing the novel CD8 T cell clone to a conventional CD8 CTL clone specific for MHC class I Kbm1 suggested that the TCR signaling pathway responsible for cyclosporine-resistance utilized the Aryl Hydrocarbon Receptor (AHR). Two T cell clones x 2 experimental conditions x 4 replicates

2014-04-14 | E-GEOD-46122 | biostudies-arrayexpress

Genome-wide analysis of gene expression regulated by calcineurin-NFAT signaling in mouse embryonic stem cells

2011-01-01 | E-GEOD-21378 | biostudies-arrayexpress

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