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Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts

ABSTRACT: BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), and the absence of TSG-6 further increases susceptibility and local inflammatory reactions, including neutrophil invasion into the joints. To gain insight into the mechanisms of TSG-6 action, synovial fibroblasts were isolated from wild-type and TSG-6-KO mice, cultured and exposed to various agents affecting either the TSG-6 expression and/or modify the intracellular function of TSG-6. In the present microarray studies, we have identified differences in gene expression by fibroblasts isolated from wild-type or TSG-6-KO mice Keywords: Genetic modification

ORGANISM(S): Mus musculus

PROVIDER: GSE17160 | GEO | 2011/07/05

SECONDARY ACCESSION(S): PRJNA119657

REPOSITORIES: GEO

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Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts

Project description:BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), and the absence of TSG-6 further increases susceptibility and local inflammatory reactions, including neutrophil invasion into the joints. To gain insight into the mechanisms of TSG-6 action, synovial fibroblasts were isolated from wild-type and TSG-6-KO mice, cultured and exposed to various agents affecting either the TSG-6 expression and/or modify the intracellular function of TSG-6. In the present microarray studies, we have identified differences in gene expression by fibroblasts isolated from wild-type or TSG-6-KO mice Keywords: Genetic modification In this study we compared the gene expression profile of 42 fibroblast cultures from mouse synovial samples. Fifteen samples were wild-type and 27 samples were TSG-6 knockout. In these two genotype groups fibroblasts were treated with TNFa, LPS, TSG-6, HA, or HA+TSG-6, and were compared to untreated samples in the same genotype group. We also compared the same treatments between KO and WT.

2011-07-04 | E-GEOD-17160 | biostudies-arrayexpress

Identification of spondylarthropathy-specific genes in BALB/c mice with proteoglycan-induced spondylitis (PGIS)

Project description:BALB/c mice develop peripheral arthritis (PGIA) and spondyloarthropathy (PGIS) upon repeated intraperitoneal injections of human cartilage proteoglycan (PG) aggrecan. The aim of the present study was to identify spondylitis-specific genes by comparing intervertebral disc (IVD) RNA samples from spondyloarthropathic and naïve BALB/c mice. Keywords: Genetic modification

2014-04-01 | GSE13782 | GEO

Transcription profiling of BALB/c mice genetically susceptible to proteoglycan-induced arthritis and spondylitis

Project description:BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), a murine model of rheumatoid arthritis (Glant,T.T. and Mikecz,K., Proteoglycan aggrecan-induced arthritis. A murine autoimmune model of rheumatoid arthritis. Methods Mol.Med. 2004. 102: 313-338.). However, there are marked differences among BALB/c colonies (maintained by different vendors at different locations) in PGIA onset and severity, which could be the result of subtle variations in their genetic background. In the present microarray study, we have identified differences among BALB/c colonies, and an altered immunization-related gene expression pattern in PGIA model. Experiment Overall Design: In this study we compared the gene expression profile of 12 spleens from PG-immunized (RNA was isolated 12 days after immunization) and naive mice from BALB/cJ and BALB/cByJ colonies (3-3 from each group), then made comparisons between colonies and based on immunization.

2009-02-21 | E-GEOD-13730 | biostudies-arrayexpress

BALB/c mice genetically susceptible to proteoglycan-induced arthritis and spondylitis

2009-02-15 | GSE13730 | GEO

Identification of spondylarthropathy-specific genes in BALB/c mice with proteoglycan-induced spondylitis (PGIS)

2014-04-01 | E-GEOD-13782 | biostudies-arrayexpress

TSG-6 mediated extracellular matrix modifications regulate hypoxic-ischemic brain injury

Project description:Proteoglycans containing link-domains modify the extracellular matrix (ECM) to regulate cellular homeostasis and can also sensitize tissues/organs to injury and stress. Hypoxic-Ischemic (H-I) injury disrupts cellular homeostasis by activating inflammation and attenuating regeneration and repair pathways. In the brain, the main component of the ECM is the glycosaminoglycan (GAG), Hyaluronic Acid (HA), but whether HA modifications of the ECM regulate cellular homeostasis and response to H-I injury is not known. In this report, employing both male and female mice, we demonstrate that link-domain containing proteoglycan, TNF-stimulated gene-6 (TSG-6), is active in the brain from birth onwards and differentially modifies ECM HA during discrete neurodevelopmental windows. ECM HA modification by TSG-6 enables it to serve as a developmental switch to regulate activity of the Hippo pathway effector protein, Yes Associated Protein 1 (YAP1) in the maturing brain and in response to H-I injury. Mice that lack TSG-6 expression display dysregulated expression of YAP1 targets, excitatory amino acid transporter 1 (EAAT1; GLAST) and 2 (EAAT2; GLT-1). Dysregulation of YAP1 activation in TSG-6-/- mice coincides with age- and sex-dependent sensitization of the brain to H-I injury such that 1-week-old neonates display an anti-inflammatory response in contrast to an enhanced pro-inflammatory injury reaction in 3-month-old adult males but not females. Our findings thus support that a key regulator of age- and sex-dependent H-I injury response in the mouse brain is modulation of the Hippo-YAP1 pathway by TSG-6 dependent ECM modifications.

2024-04-09 | GSE249085 | GEO

RNAseq of epidermis reconstructed from TSG-6-/- and TSG-6+/+ immortalized N/TERT keratinocytes and stimulated or not with interleukins 4 and 13 for 48h

Project description:TNFα-stimulated gene 6 (TSG-6) is an anti-inflammatory protein. In human epidermis, TSG-6 is secreted in extracellular matrix where it interacts with hyaluronan (HA). However, their functions are not well understood. In this study, immortalized N/TERT keratinocytes were edited by CRISPR/Cas9, used to reconstruct in vitro epidermis (RHE) and stimulated or not with interleukins 4 and 13 for 48h to mimic atopic dermatitis (AD). Two TSG-6-/- clones (respectively TSG-6-/- (a) and TSG-6-/- (b)) harboring major deletions in both alleles were selected and compared to TSG-6+/+ cells. Epidermis reconstructed from TSG-6-/- (a) and TSG-6-/- (b) exhibit normal differentiation process and morphology but show an increased HA leakage in the underlying culture medium of both TSG-6-/- RHE compared to TSG-6+/+ tissues, especially in conditions that mimic AD. While IL-4/13 treatment of RHE induces regulation of genes associated with AD, the absence of TSG-6 don’t seem to show any major transcriptomic regulation.

2021-12-30 | E-MTAB-10095 | biostudies-arrayexpress

TSG-6 supports fistulizing Crohn’s disease by a mechanoregulated activation of the epithelial-to-mesenchymal transition

Project description:BACKGROUND AND AIMS: Perianal fistula represents one of the most important complications in Crohn’s Disease (CD). Epithelial-to-mesenchymal transition (EMT) has been demonstrated to play a major role in the pathogenesis, however the mechanisms driving EMT need to be clarified. Significant alterations in the tissue structural composition occur in the fistula, but how these changes promote EMT was not addressed. We aim to explore the relevance of TSG-6, a stabilizer of extracellular matrix, in the fistula pathogenesis. METHODS: Intestinal surgical specimens from perianal fistula tissue and surrounding region of fistulizing CD were analyzed histologically and by RNA sequencing (RNA-seq). Significantly modulated genes and TSG-6 expression were validated by RT-PCR, WB and immunofluorescence assays [N=20]. TSG-6 expression was reconstituted in Caco-2 cell line and primary perifistula-derived fibroblasts, and proliferative and migratory assays were performed. RESULTS: A marked different organization of extracellular matrix was found across fistula and perifistula regions with an increased expression of integrins, hyaluronan synthases, TSG-6 and MMPs in the fistula. TSG-6 overexpression in Caco-2 cells reduced proliferation, promoted the EMT transcription factor SNAIL, and, in co-stimulation with TGFβ1, migration. The acquisition of TSG-6 increased SNAI1 and hyaluronan synthases levels, and led to activated phenotype of perifistula-derived fibroblasts. Positive Pearson correlation was observed between TSG-6 expression and mechanosensitive proteins in fistula tissue. CONCLUSIONS: By mediating changes in the extracellular matrix organization, TSG-6 triggers the EMT transcription factor SNAIL through the activation of mechanosensitive proteins. These data point to TSG-6 as a new potential target for the treatment of perianal fistula.

2023-01-04 | GSE157020 | GEO

Transcriptome changes after TSG-6 treatment of mouse liver fibrosis.

Project description:Our previous studies revealed that exogenous administration of TSG-6 can ameliorate liver fibrosis. We next analyzed liver transcriptome changes after TSG-6 treatment in order to explore possible therapeutic changes.

2021-10-23 | GSE121669 | GEO

Co-IP/MS for determining interacting partners of TSG-6 in human pHSCs

Project description:Interacting partners of TSG-6 were analyzed by coimmunoprecipitation (co-IP) coupled with liquid chromatography tandem mass spectrometry (LC–MS/MS)

2024-06-16 | PXD047449 | Pride

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