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RNA-seq analysis of IL-10 treatment of wildtype and Ptpn1-/- knockout peritoneal macrophages

ABSTRACT: We report here the deep sequencing of the mRNA from peritoneal exudate cells (macrophages) purified from wildtype or Ptpn1 (PTP1B) knockout mice, either treated or untreated with IL-10. In periotenal macrophages IL-10 activates the transcription factor STAT3 to execute and anti-inflammatory gene expression programme. The tyrosine phosphatase PTPN1 targets STAT3 for dephosphorylation and leads to the deactivation of STAT3. In this study we examined the role of PTP1B in controlling the normal homeostatic level phosphorylation of STAT3 by comparing the IL-10/STAT3-mediated anti-inflammatory gene expression programme. We find that loss of PTP1B leads to an up-regulation of the activity of STAT3, both at the level of phosphorylation and also in enhanced expression of anti-inflammatory gene products.

ORGANISM(S): Mus musculus

PROVIDER: GSE49449 | GEO | 2014/05/12

SECONDARY ACCESSION(S): PRJNA213962

REPOSITORIES: GEO

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RNA-seq analysis of IL-10 treatment of wildtype and Ptpn1-/- knockout peritoneal macrophages

Project description:We report here the deep sequencing of the mRNA from peritoneal exudate cells (macrophages) purified from wildtype or Ptpn1 (PTP1B) knockout mice, either treated or untreated with IL-10. In periotenal macrophages IL-10 activates the transcription factor STAT3 to execute and anti-inflammatory gene expression programme. The tyrosine phosphatase PTPN1 targets STAT3 for dephosphorylation and leads to the deactivation of STAT3. In this study we examined the role of PTP1B in controlling the normal homeostatic level phosphorylation of STAT3 by comparing the IL-10/STAT3-mediated anti-inflammatory gene expression programme. We find that loss of PTP1B leads to an up-regulation of the activity of STAT3, both at the level of phosphorylation and also in enhanced expression of anti-inflammatory gene products. RNA-seq of wildtype and Ptpn1 (PTP1B) knockout mouse peritoneal macrophages, treated or untreated with IL-10

2014-05-12 | E-GEOD-49449 | biostudies-arrayexpress

A Bartonella effector acts as signaling hub for intrinsic STAT3 activation to trigger anti-inflammatory responses

Project description:Chronically infecting pathogens avoid clearance by the innate immune system by promoting premature transition from an initial pro-inflammatory response towards an anti-inflammatory tissue-repair response. STAT3, a central regulator of inflammation, controls this transition and thus is targeted by numerous chronic pathogens. Here we show that BepD, an effector of the chronic bacterial pathogen Bartonella henselae targeted to infected host cells, establishes an exceptional pathway for canonical STAT3 activation, thereby impairing secretion of pro-inflammatory TNF-α and stimulating secretion of anti-inflammatory IL-10. Tyrosine phosphorylation of EPIYA-related motifs in BepD facilitates STAT3 binding and activation via c-Abl-dependent phosphorylation of Y705. The tyrosine-phosphorylated scaffold of BepD thus represents a signaling hub for intrinsic STAT3 activation that is independent from canonical STAT3 activation via transmembrane receptor-associated Janus kinases. We anticipate that our findings on a molecular shortcut to STAT3 activation will inspire new treatment options for chronic infections and inflammatory diseases.

2020-02-12 | PXD017119 | Pride

Transcription profiling of mouse IL-10 -/- macrophages treated with LPS/LPS plus IL10 reveals a transcriptional repressor and co-repressor induced by the STAT3-regulated anti-inflammatory signaling pathway.

Project description:IL-10 regulates anti-inflammatory signaling via the activation of STAT3, which in turn controls the induction of a gene expression program whose products execute inhibitory effects on pro-inflammatory mediator production. Here we show that IL-10 induces the expression of an ETS family transcriptional repressor, ETV3 and a helicase family co-repressor, SBNO2 (Strawberry notch homolog 2) in mouse and human macrophages. IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3, and co-stimulus through the TLR pathway. We also observed that ETV3 expression was strongly induced by the STAT3 pathway induced by IL-10 but not STAT3 signaling activated by IL-6, which cannot activate the anti-inflammatory signaling pathway. ETV3 and SBNO2 specifically repressed NF-kB-mediated transcription and can physically interact. Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10. We compared expression profiles of macrophages isolated from IL-10 -/- mice. Macrophages were treated with either LPS or LPS plus IL-10. Treatment times were 10, 20 and 30 minutes. Experiment Overall Design: Mouse IL-10 -/- macrophages were isolated and purified and set up in culture medium containing LPS or LPS plus IL-10. A total of 18 samples were analyzed. This set contains three replicates of each treatment condition where treatment (LPS versus LPS plus IL-10) and time (10min, 20min and 30min) were varied.

2008-06-16 | E-GEOD-9509 | biostudies-arrayexpress

A transcriptional repressor and co-repressor induced by the STAT3-regulated anti-inflammatory signaling pathway.

Project description:IL-10 regulates anti-inflammatory signaling via the activation of STAT3, which in turn controls the induction of a gene expression program whose products execute inhibitory effects on pro-inflammatory mediator production. Here we show that IL-10 induces the expression of an ETS family transcriptional repressor, ETV3 and a helicase family co-repressor, SBNO2 (Strawberry notch homolog 2) in mouse and human macrophages. IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3, and co-stimulus through the TLR pathway. We also observed that ETV3 expression was strongly induced by the STAT3 pathway induced by IL-10 but not STAT3 signaling activated by IL-6, which cannot activate the anti-inflammatory signaling pathway. ETV3 and SBNO2 specifically repressed NF-kB-mediated transcription and can physically interact. Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10. We compared expression profiles of macrophages isolated from IL-10 -/- mice. Macrophages were treated with either LPS or LPS plus IL-10. Treatment times were 10, 20 and 30 minutes. Keywords: time-course, treatment response, gene expression analysis

2007-12-01 | GSE9509 | GEO

GENE EXPRESION PROFILE OF HEPATIC PROGENITOR CELLS FROM Ptpn1+/+ AND Ptpn1-/- MICE AFTER PALMITIC ACID TREATMENT

Project description:We report the role of PTP1B deficiency in hepatic progenitor cells in the protection against lipotoxic injury

2022-04-01 | GSE199644 | GEO

Expression changes induced by PTPN1 knockdown in KM-H2 cells

Project description:Gene expression data for shRNA PTPN1 knockdown vs. Non-silencing in the classical Hodgkin lymphoma-derived cell line KM-H2

2014-01-17 | GSE54157 | GEO

Expression changes induced by PTPN1 knockdown in KM-H2 cells

Project description:Gene expression data for shRNA PTPN1 knockdown vs. Non-silencing in the classical Hodgkin lymphoma-derived cell line KM-H2 A total of 4 samples were analyzed (2 Knockdown vs. 2 Non-silencing). The 2 knockdown and 2 non-silencing samples are technical replicates of each other.

2014-01-17 | E-GEOD-54157 | biostudies-arrayexpress

GENE EXPRESION PROFILE OF HEPATIC PROGENITOR CELLS FROM Ptpn1+/+ AND Ptpn1-/- MICE AFTER PALMITIC ACID TREATMENT

Project description:GENE EXPRESION PROFILE OF HEPATIC PROGENITOR CELLS FROM Ptpn1+/+ AND Ptpn1-/- MICE AFTER PALMITIC ACID TREATMENT

| PRJNA821058 | ENA

Salmonella activation of STAT3 signaling by SarA effector promotes intracellular replication and production of IL-10

Project description:Salmonella enterica is an important foodborne pathogen that utilizes secreted effector proteins to manipulate host pathways to facilitate survival and dissemination. Different S. enterica serovars cause disease syndromes ranging from self-limited gastroenteritis to typhoid fever and vary in their repertoire of effectors. We leveraged this natural diversity to identify stm2585, here designated sarA (Salmonella anti-inflammatory response activator), as a Salmonella effector secreted primary by the SPI-2 type III secretion system. SarA is necessary and sufficient to induce STAT3 phosphorylation and IL-10 production, contributing to intracellular replication in vitro and bacterial load at systemic sites in mice. These results demonstrate that Salmonella has evolved effector mechanisms for regulating a host anti-inflammatory signaling pathway important in infection, autoimmunity, and cancer.

2018-06-01 | GSE104354 | GEO

STAT3 Inhibits Autocrine Interferon Signaling in Type I Conventional Dendritic Cells

Project description:Type I conventional dendritic cells (cDC1s) are an essential antigen-presenting population, required for generating adaptive immunity against intracellular pathogens and tumors. While the transcriptional control of cDC1 development is well understood, the mechanisms by which extracellular stimuli affect cDC1 function remain unclear. Recently, we demonstrated that the cytokine IL-10 inhibits cDC1 maturation induced upon polyinosinic-polycytidylic acid (poly I:C) exposure via a STAT3-dependent mechanism. Furthermore, utilizing a tumor vaccine strategy, we found STAT3 restrains cDC1-mediated anti-tumor immunity. To understand the pathways by which IL-10 and STAT3 regulate cDC1s, we evaluated transcriptional responses by RNA-sequencing. Bioinformatic analyses indicated that many inflammatory pathways were enriched in cDC1s following poly I:C treatment, while interferon (IFN) signaling was uniquely inhibited by STAT3 upon concomitant exposure to IL-10. We found that poly I:C stimulated production of IFN-b and IFN-g from cDC1s. Concurrent exposure to IL-10 suppressed IFN-b and IFN-g secretion as well as accrual of phosphorylated STAT1 and expression of the IFN-response gene Cxcl10 in cDC1s. By contrast, Stat3-deficient cDC1s were refractory to IL-10, indicating STAT3 controls poly I:C-mediated IFN production and IFN transcriptional responses in cDC1s. Moreover, we found that maturation of cDC1s in response to poly I:C is dependent on the type I IFN receptor. Taken together, our data indicate STAT3 is essential for restraining autocrine type I IFN signaling in cDC1s elicited by poly I:C stimulation.

2022-07-26 | GSE188995 | GEO

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