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Analysis of gene expression during glucocorticoid-induced apoptosis of rat primary thymocytes

ABSTRACT: Glucocorticoids induce rapid apoptosis of rat primary thymocytes through mechanisms requiring altered gene expression. The determination of genes regulating glucocorticoid-induced apoptosis of lymphocytes has received considerable attention. However, the role of specific non-coding microRNAs in the regulation of glucocorticoid-induced apoptosis of lymphocytes is poorly defined. Using deep sequencing analysis, we have identified microRNAs differentially expressed during glucocorticoid-induced apoptosis of rat primary thymocytes. We have also identified numerous loci that harbor probable novel microRNAs. Furthermore, we have validated the glucocorticoid-responsive expression of 2 novel microRNAs in the apoptotic rat primary thymocyte. These 2 novel microRNAs are predicted to target numerous messenger RNAs throughout the genome. Using whole genome expression analysis, we now seek to correlate the altered expression of these novel microRNAs with the expression of their predicted target mRNAs during glucocorticoid-induced apoptosis.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE45560 | GEO | 2014/03/26

SECONDARY ACCESSION(S): PRJNA194577

REPOSITORIES: GEO

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Analysis of gene expression during glucocorticoid-induced apoptosis of rat primary thymocytes

Project description:Glucocorticoids induce rapid apoptosis of rat primary thymocytes through mechanisms requiring altered gene expression. The determination of genes regulating glucocorticoid-induced apoptosis of lymphocytes has received considerable attention. However, the role of specific non-coding microRNAs in the regulation of glucocorticoid-induced apoptosis of lymphocytes is poorly defined. Using deep sequencing analysis, we have identified microRNAs differentially expressed during glucocorticoid-induced apoptosis of rat primary thymocytes. We have also identified numerous loci that harbor probable novel microRNAs. Furthermore, we have validated the glucocorticoid-responsive expression of 2 novel microRNAs in the apoptotic rat primary thymocyte. These 2 novel microRNAs are predicted to target numerous messenger RNAs throughout the genome. Using whole genome expression analysis, we now seek to correlate the altered expression of these novel microRNAs with the expression of their predicted target mRNAs during glucocorticoid-induced apoptosis. Changes in gene expression during glucocorticoid-induced apoptosis of rat primary thymocyes (3 biological replicates) were measured after 6 hours of 100nM dexamethasone treatment in-vitro.

2014-03-26 | E-GEOD-45560 | biostudies-arrayexpress

Rattus norvegicus

Project description:Analysis of gene expression during glucocorticoid-induced apoptosis of rat primary thymocytes

| PRJNA194577 | ENA

Expression data in KSHV-infected primary rat mesenchymal precursor (MM) cells

Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) can efficiently infect and transform primary rat mesenchymal precursor (MM) cells. Regulation of cell cycle progression and apoptosis by KSHV-encoded microRNAs is required for KSHV-induced cellular transformation and tumorigenesis.

2013-08-28 | GSE50381 | GEO

Assessing the role of microRNAs in post-transcriptional control of thymocytes and peripheral lymphocytes in NOD mice

Project description:As early as one month of age, non-obese diabetic (NOD) mice feature pancreatic infiltration of autoreactive T lymphocytes, which destruct insulin-producing beta cells, leading to autoimmune diabetes mellitus (T1D) within eight months. Thus, we hypothesized that during the development of T1D, the transcriptional modulation of immune reactivity genes, as well as, modulation of microRNAs (miRNAs) may occur during thymocytes mature into peripheral CD3+ T lymphocytes. Our aim is to analyze the transcriptional modulation of mRNA and microRNAs during development of thymocytes into peripheral CD3+ T lymphocytes in the context of the emergence of T1D.

2011-07-01 | E-MEXP-3235 | biostudies-arrayexpress

Transcription profiling of human pretreatment glucocortocoid sensitive and resistant primary leukaemias

Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. Experiment Overall Design: primary acute lymphoblastic leukemia samples were determined to be sensitive or resistant to in vitro treatment with glucocorticoids. Samples were then hybrized to affymetrix microarrays

2009-04-04 | E-GEOD-5820 | biostudies-arrayexpress

Transcription profiling of rat kidney samples from Dahl SS/J and Sprague Dawley animals placed on high salt and basal salt diets

Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithselial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat.

2007-10-11 | E-GEOD-599 | biostudies-arrayexpress

Dietary salt and renal function

Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithelial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat. Keywords = Rattus norvegicus, Sprague Dawley, Dahl SS/Jr, kidney, NaCl diet Keywords: other

2004-02-14 | GSE599 | GEO

Transcription profiling of thymic mouse cells

Project description:Glucocorticoids (GC) are in most chemotherapy protocols for lymphoid malignancies, particularly childhood acute lymphoblastic leukaemia (ALL) for their ability to induce apoptosis in malignant blast. The underlying mechanism, however, has so far only been investigated in model systems. This study comprises Affymetrix hgu133 plus 2.0 analyses of; Peripheral blood lymphoblasts purified at three time points (0h, 6-8h, 24h after treatment initiation) from 13 children under therapy for ALL . Treated samples were compared to untreated (0h). For comparison, expression profiles were generated from an adult ALL patient, peripheral blood lymphocytes from GC-exposed healthy donors, GC-sensitive and -resistant ALL cell lines and mouse thymocytes treated with GC in vivo and in vitro. This series consists of the mouse thymocyte samples. Findings. An essentially complete list of GC-regulated candidate genes in clinical settings experimental and was generated, enabling immediate analysis of any gene with respect to its potential significance for GC-induced apoptosis in these systems. Gene regulations previously thought responsible for cell death in experimental systems were reconfirmed in few children only. In contrast, a small number of genes, most not implicated in GC-induced apoptosis previously, were co-ordinately regulated in the majority of children. Experiment Overall Design: In vivo and in vitro glucocorticoid treated samples were compared to their control samples (ethanol or PBS treated).

2008-06-12 | E-GEOD-2843 | biostudies-arrayexpress

Development of type 1 diabetes mellitus T1D in NOD mice follows transcriptional activity of thymocytes and peripheral T lymphocytes

Project description:Non-obese diabetic (NOD) mice feature pancreatic infiltration of autoreactive T lymphocytes as early as 1 month of age, which destruct insulin-producing beta-cells to finally emerge autoimmune diabetes mellitus (T1D) within 8 months. In view, we hypothesized that during the development of T1D, transcriptional modulation of immune reactivity genes may occur as thymocytes mature toward peripheral T lymphocytes. Transcriptome of thymocytes and peripheral CD3+ T lymphocytes from pre-diabetic or diabetic mice analyzed through microarray hybridizations allowed observation of 3,586 differentially expressed genes. Hierarchical clustering grouped mice according to age/T1D onset and genes to their ontology. Transcriptional activity of thymocytes toward peripheral T lymphocytes unraveled sequential participation of genes involved with CD4+/CD8+ T cell differentiation (Themis), tolerance induction (Foxp3), apoptosis (Fasl) to soon after T cell activation (IL4), while the emergence of T1D coincided with the expression of cytotoxicity (Crtam) and inflammatory response genes (Tlr) by peripheral T lymphocytes.

2011-03-03 | E-MEXP-3047 | biostudies-arrayexpress

Transcription profiling of thymocytes from Kruppel-like transcription factor (KLF)13 knock-out mice

Project description:Kruppel-like transcription factor (KLF)13, previously shown to regulate RANTES expression in vitro, is a member of the Kruppel- like family of transcription factors that controls many growth and developmental processes. To ascertain the function of KLF13 in vivo, Klf13-deficient mice were generated by gene targeting. As expected, activated T lymphocytes from Klf13-/- mice show decreased RANTES expression. However, these mice also exhibit enlarged thymi and spleens. TUNEL, as well as spontaneous and activation-induced death assays, demonstrated that prolonged survival of Klf13-/- thymocytes was due to decreased apoptosis. Microarray analysis suggests that protection from apoptosis-inducing stimuli in Klf13-/- thymocytes is due in part to increased expression of BCL-XL, a potent antiapoptotic factor. This finding was confirmed in splenocytes and total thymocytes by real-time quantitative PCR and Western blot as well as in CD4+CD8? single-positive thymocytes by real-time quantitative PCR. Furthermore, EMSA and luciferase reporter assays demonstrated that KLF13 binds to multiple sites within the Bcl-XL promoter and results in decreased Bcl-XL promoter activity, making KLF13 a negative regulator of BCL-XL.

2007-05-11 | E-SMDB-4035 | biostudies-arrayexpress

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