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HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [TSA exp]

ABSTRACT: Analysis of the effect of HDAC inhibitor TSA on IL-1-induced gene expression in SW1353 chondrocytes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE186689 | GEO | 2021/10/29

REPOSITORIES: GEO

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HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [HDAC siRNA exp]

Project description:Analysis of the effect of HDAC6 knockdown on IL-1-induced gene expression in SW1353 chondrocytes.

2021-10-29 | GSE186688 | GEO

HDAC6 regulates NF-κB signalling to control chondrocyte IL-1-induced MMP and inflammatory gene expression.

Project description:Elevated pro-inflammatory signalling coupled with catabolic metalloproteinase expression is a common feature of arthritis, leading to cartilage damage, deterioration of the joint architecture and the associated pain and immobility. Countering these processes, histone deacetylase inhibitors (HDACi) have been shown to suppress matrix metalloproteinase (MMP) expression, block cytokine-induced signalling and reduce the cartilage degradation in animal models of the arthritis. In order to establish which specific HDACs account for these chondro-protective effects an HDAC1-11 RNAi screen was performed. HDAC6 was required for both the interleukin (IL)-1 induction of MMP expression and pro-inflammatory interleukin expression in chondrocytes, implicating an effect on NF-κB signalling. Depletion of HDAC6 post-transcriptionally up-regulated inhibitor of κB (IκB), prevented the nuclear translocation of NF-κB subunits and down-regulated NF-κB reporter activation. The pharmacological inhibition of HDAC6 reduced MMP expression in chondrocytes and cartilage collagen release. This work highlights the important role of HDAC6 in pro-inflammatory signalling and metalloproteinase gene expression, and identifies a part for HDAC6 in the NF-κB signalling pathway. By confirming the protection of cartilage this work supports the inhibition of HDAC6 as a possible therapeutic strategy in arthritis.

| S-EPMC9033835 | biostudies-literature

HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [TSA exp]

Project description:HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [TSA exp]

| PRJNA775078 | ENA

HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-10-29 | GSE186690 | GEO

HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [HDAC siRNA exp]

Project description:HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [HDAC siRNA exp]

| PRJNA775079 | ENA

Effect of HDAC inhibitor TSA on haploid embryogenesis [dataset 1]

Project description:Haploid embryos can be induced from cultured immature pollen following a stress treatment. In Brassica napus, application of the histone/lysine deacetylase (HDAC/KDAC) inhibitor trichostatin A (TSA) to pollen cultures enhances the production of differentiated embryos and embryogenic callus when applied together with heat stress (Li et al., 2014). To identify genes associated with the induction of B. napus haploid embryogenesis, we compared the transcriptomes of untreated pollen cultures and pollen cultures treated with either heat-stress or heat-stress plus TSA.

2020-08-03 | GSE140969 | GEO

HDAC inhibition by TSA and Butyrate In Flt3L-elicited DC

Project description:Butyrate induces Treg via HDACi activity Microarray of DC treated with TSA or Butyrate over untreated

2013-10-15 | E-GEOD-51263 | biostudies-arrayexpress

The activation of inflammatory response genes by LPS is blocked by HDAC inhibitor Trichostatin A (TSA)

Project description:TSA treatment blocks LPS-induction of several inflammatory target genes in primary macrophages. The microarray experiment was performed to identify LPS-inducible, LXR-sensitive target genes that retained LPS-induction in the presence of TSA. Thioglycollate-elicited macrophages were isolated from mice by peritoneal lavage 3 days following peritoneal injection of 2.5 ml 3% thioglycollate (DIFCO). Cells were plated in RPMI medium 1640 and 10% fetal bovine serum, washed after 5 h the medium was removed and cells were fed with fresh medium containing 0.5% fetal bovine serum. Cells were treated with TSA (Wako) at 100nM and/or with LPS (Sigma) at concentration of 100 ng/ml in the absence or presence of receptor-specific agonist for LXR (GW3965) at 1 µM. Keywords: TSA, LPS, LXR agonist

2006-12-15 | GSE6352 | GEO

Vascular histone deacetylation by pharmacological HDAC inhibition [TSA, RNA-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC mRNA profiles of TSA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-37376 | biostudies-arrayexpress

Vascular histone deacetylation by pharmacological HDAC inhibition [TSA, ChIP-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC ChIP-seq profiles for 3 histone marks of TSA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-37377 | biostudies-arrayexpress

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