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Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis

ABSTRACT: Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis

PROVIDER: PRJNA976361 | ENA |

REPOSITORIES: ENA

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Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [adipose_scRNAseq]

Project description:Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [adipose_scRNAseq]

| PRJNA976397 | ENA

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [synovium_scRNA-seq]

Project description:Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [synovium_scRNA-seq]

| PRJNA976395 | ENA

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [fibroblast_bulk RNAseq]

Project description:Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [fibroblast_bulk RNAseq]

| PRJNA976396 | ENA

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [adipose_scRNAseq]

Project description:Fibroblasts play critical roles in tissue homeostasis, but in pathologic states can drive fibrosis, inflammation, and tissue destruction. In the joint synovium, fibroblasts provide homeostatic maintenance and lubrication. Little is known about what regulates the homeostatic functions of fibroblasts in healthy conditions. We performed RNA sequencing of healthy human synovial tissue and identified a fibroblast gene expression program characterized by enhanced fatty acid metabolism and lipid transport. We found that fat-conditioned media reproduces key aspects of the lipid-related gene signature in cultured fibroblasts. Fractionation and mass spectrometry identified cortisol in driving the healthy fibroblast phenotype, confirmed using glucocorticoid receptor gene (NR3C1) deleted cells. Depletion of synovial adipocytes in mice resulted in loss of the healthy fibroblast phenotype and revealed adipocytes as a major contributor to active cortisol generation via Hsd11β1 expression. Cortisol signaling in fibroblasts mitigated matrix remodeling induced by TNFα- and TGFβ, while stimulation with these cytokines repressed cortisol signaling and adipogenesis. Together, these findings demonstrate the importance of adipocytes and cortisol signaling in driving the healthy synovial fibroblast state that is lost in disease.

2024-08-08 | GSE233500 | GEO

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [fibroblast_bulk RNAseq]

2024-08-08 | GSE233501 | GEO

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [synovium_scRNA-seq]

2024-08-08 | GSE233502 | GEO

Regulation of synovial DKK1 expression by local glucocorticoid metabolism in inflammatory arthritis

Project description:Inflammatory arthritis is associated with bone loss and fractures due to abnormal bone remodelling. Bone remodelling is 'uncoupled' with bone resorption increased and bone formation suppressed. These changes resemble those seen in patients treated with therapeutic glucocorticoids, and in both of these situations, altered wnt signalling is implicated. Recent studies have highlighted the importance of the synovial fibroblast in mediating abnormal bone remodelling during inflammation. The wnt antagonist dickkopf-1 (DKK1) is secreted by synovial fibroblasts in response to inflammation, and this protein has been proposed to be a master regulator of bone remodelling in inflammatory arthritis. Here we show that DKK1 expression by primary human synovial fibroblasts is more potently regulated by glucocorticoids than pro-inflammatory cytokines. Glucocorticoids, but not TNF-alpha, regulated expression of multiple wnt agonists and antagonists in favour of inhibition of wnt signalling. In vitro TNF-alpha and IL1-beta indirectly regulate DKK1 production through increased expression of the glucocorticoid activating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). These results demonstrate that the links between synovial inflammation, altered wnt signalling and bone remodelling may not be direct but are dependent on local activation of endogenous glucocorticoids. Human fibroblast-like synoviocytes isolated from patients with rheumatoid arthritis treated with either vehicle, TNF or dexamethasone (dex). Gene arrays for control, TNF and dexamethasone treatments were performed on three separate synovial fibroblast cell lines isolated from three rheumatoid arthritis patients. All fold changes displayed are the combined results of the three separate fibroblast lines.

2012-04-24 | E-GEOD-37520 | biostudies-arrayexpress

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis

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

2024-08-08 | GSE233504 | GEO

Direct cell conversion from human dermal fibroblast to adipocyte

Project description:To investigate the effect of ZNF395 on adipogenesis, we tested whether ZNF395 enhance cell conversion from human dermal Fibroblast (FIB) to Adipocyte (ADP). PPARG2 was reported as a master regulator and can induce adipogenesis in non-adipogenic fibroblasts. We transduced PPARG2 with or without ZNF395 in FIB with lentivirus. Interestingly, co-transduction of PPARG2 and ZNF395 showed higher occurrence of adipocyte-like cells as compared with PPARG2 alone. Moreover, genes related with lipid metabolic process and lipid transport was significantly up-regulated in combination of PPARG2 and ZNF395. These results suggest that ZNF395 co-ordinate the transcriptional regulatory pathway with PPARG2, necessary for the induction of adipogenesis. Total RNA was obteined from human dermal fibroblast transduced with mock lentivirus vector (FIB_ctrl), PPARG2 (FIB_PPARG2) and co-transduced with PPARG2 and ZNF395 (FIB_PPARG2+ZNF395).

2012-12-01 | E-GEOD-37925 | biostudies-arrayexpress

lncRNA and mRNA expression profiles in fibroblast-like synoviocytes from rheumatoid arthritis patients and trauma patients

Project description:Fibroblast-like synoviocytes (FLSs) are critical for synovial aggressiveness and joint destruction in rheumatoid arthritis (RA).The role and expression patterns of long noncoding RNAs (lncRNAs) in RA are largely unknown. We performed lncRNA and mRNA microarrays to identify differentially expressed lncRNAs and mRNAs in fibroblast-like synoviocytes from rheumatoid arthritis patients compared with fibroblast-like synoviocytes from trauma patients.

2018-09-07 | GSE103578 | GEO

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