Expression data from IMR90 cells expressing either E7-ca-STAT5A-shNTC vs E7-ca-STAT5a-shSOCS1 at 7 days post infection
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE98216 | GEO | 2017/11/07
SECONDARY ACCESSION(S): PRJNA384317
REPOSITORIES: GEO
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Project description:Stat5+/- mice were bred into the C57BL/6 background. Stat5+/- mice were intercrossed and mouse embryonic fibroblasts (MEFs) were isolated from 12.5-13.5-day WT or Stat5-/- fetuses. The retroviral-expression vector carrying a DNA binding domain mutant Stat5A (E437/E438?AA) or tyrosine-phosphorylated Stat5A Y694F mutation based on an MSCV-IRES-GFP backbone (gift from Richard Moriggl, Ludwig-Boltzmann Institute, Vienna, Austria) was infected into Stat5-/- MEFs. FACS was used to select GFP+ cells. After 5 hours starvation in serum free medium with 0.1% of BSA, MEFs were treated with growth hormone for 2 hours. Total cellular RNA from each group of the MEFs was extracted with TRIzol reagent (Invitrogen) according to the manufacturer's instructions. Microarray analyses were performed using Affymetrix Mouse Genome 430 2.0 GeneChips (Affymetrix, Santa Clara, CA) (four groups, biological replicates for each group). Expression values were determined with GeneChip Operating Software (GCOS) v1.1.1 software. RMA signals were summarized using GeneSpring GX 10.0.1 (Agilent) and normalized by quantile normalization. All data analysis was performed with GeneSpring software GX 10.01. Total 4 groups (EA, EA_GH, YF, YF_GH), biological duplicate replication for each group
2013-11-12 | E-GEOD-33770 | biostudies-arrayexpress
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Project description:We assessed the gene expression profiles induced by both genetic and pharmacological knockdown of Stat5a/b in CML cells. Stat5 was suppressed in K562 cells by lentiviral expression of Stat5 shRNA vs. scramble control for 6 days or by treatment of the cells with IST5-002 (5 µM) for 48 h. K562 cells were treated with IST5-002 (5 µM) or vehicle (DMSO) for 48 h. For Stat5 knockdown, K562 cells were infected with Stat5-shRNA lentivirus or scramble-shRNA lentivirus (as control) for 48 h followed by puromycin (2ug/ml) selection for 6 days to enrich for cells expressing Stat5 or scramble shRNA. Each group (vehicle control, IST5-002, scramble-shRNA control and Stat5-shRNA) was prepared in triplicate, and RNA samples from each group were not pooled.
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Project description:The impact of STAT5 on liver DNA methylation was assessed by performing RRBS analysis on male and female mouse liver with a hepatocyte-specific loss of STAT5a and STAT5b. Extensive changes in CpG-methylation were seen in STAT5-deficient liver, where sex differences were abolished at 88% of ~1,500 sex-differentially methylated regions, largely due to increased DNA methylation upon STAT5 loss. STAT5-dependent CpG-hypomethylation was rarely found at proximal promoters of STAT5-dependent genes. Rather, STAT5 primarily regulated the methylation of distal enhancers, where STAT5 deficiency induced widespread hypermethylation at genomic regions enriched for accessible chromatin, enhancer histone marks (H3K4me1, H3K27ac), STAT5 binding, and DNA motifs for STAT5 and other transcription factors implicated in liver sex differences. Thus, the sex-dependent binding of STAT5 to liver chromatin is closely linked to the sex-dependent demethylation of distal regulatory elements linked to STAT5-dependent genes important for liver sex bias.
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Project description:rRNA-depleted RNA isolated from livers of control male and female mice and from male mice with hepatocyte-specific STAT5ab-KO was analyzed by RNA-seq. This study revealed a substantial, albeit incomplete loss of liver sex bias in hepatocyte-specific STAT5a/STAT5b (collectively, STAT5)-deficient mouse liver. Notably, in male liver, many male-biased genes were down regulated in direct association with the loss of STAT5 binding; many female-biased genes, which show low STAT5 binding, were de-repressed, indicating an indirect mechanism for repression by STAT5.
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Project description:Inhibition of STAT5 was recently reported to reduce mouse atherosclerosis. However, the regulatory role of STAT5 isoforms STAT5A and STAT5B in human disease and more specifically in macrophages remains unknown. Here, we demonstrate reciprocal expression regulation of STAT5A and B in human atherosclerotic lesions. The former was highly upregulated in ruptured over stable plaque and correlated with macrophage presence, a finding that was corroborated by the high chromosomal accessibility of STAT5A but not B gene in plaque macrophages. Phosphorylated STAT5 correlated with macrophages confirming its activation status. As macrophage STAT5 is activated by GM-CSF, we studied the effects of its silencing in GM-CSF differentiated human macrophages. STAT5A knockdown blunted NF-kB pathway, phagocytosis, cholesterol metabolism, and apoptosis terms. These changes at transcriptional level could be confirmed at functional level, with significant increases in apoptosis and phagocytosis and decreases in lipid uptake and IL-6, IL8, and TNFa cytokine secretion after STAT5A knockdown. Finally, inhibition of general and isoform A specific STAT5 inhibitor significantly reduced the secretion of TNFa, IL-8 and IL-10 in ex vivo tissue slices of advanced human atherosclerotic plaques. In summary, we identify STAT5A as important determinant of macrophage functions and inflammation in the context of atherosclerosis and show its promise as therapeutic target for human atherosclerotic plaque inflammation.
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