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Gene expression alteration in rat primary TNF-α-induced chondrocytes and the treatment of Nanofat lysate

ABSTRACT: Gene expression alteration in rat primary TNF-α-induced chondrocytes and the treatment of Nanofat lysate

PROVIDER: PRJNA822798 | ENA |

REPOSITORIES: ENA

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Gene expression alteration in rat primary TNF-α-induced chondrocytes and the treatment of Nanofat lysate

Project description:In order to overcome the defect of Nanofat, we developed Nanofat lysate (NFL) by repeated freeze-thawing lysis preparation on Nanofat. During the preparation, cell membranes of Nanofat cells were ruptured and the cellular contents were released. Thus, NFL may have storage stability in low temperature. Therefore, to investigate the effects of the stimulation of TNF-α on primary chondrocytes and the effect of NFL, we can speculate that unique genetic profiles in vitro might exist with different interventions.

2023-04-19 | GSE200058 | GEO

Osteoarthritic chondrocytes undergo a glycolysis-related metabolic switch upon exposure to IL-1β or TNF-α

Project description:Inflammation, which is mainly sustained by pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6, plays an important role in osteoarthritis progression. However, the therapeutic failures of recent clinical trials evaluating anti-IL-1, anti-TNF, and anti-IL-6 drugs highlight the lack of overall understanding of the effects of these cytokines on chondrocytes. Here, we generated a comprehensive transcriptomic and proteomic dataset of osteoarthritic chondrocytes treated with these cytokines to describe their pro-inflammatory signature and compare it to the transcriptome of non-osteoarthritic chondrocytes. We first identified specific dysregulation of metabolic-related genes in OA chondrocytes. A metabolic shift, toward increased glycolysis at the expense of mitochondrial respiration, was specifically identified and confirmed by Seahorse® assay of osteoarthritic chondrocytes treated with IL-1β or TNF-α. These data show a strong association between inflammation and metabolism, indicating that understanding metabolic dysregulations should be a focus of future investigations for the design of therapies for osteoarthritis.

2023-05-20 | GSE215039 | GEO

Gene expression in primary chondrocytes derived from Rela-cKO/control mice with/without TNF-α treatment

Project description:To identify target genes mediating the anti-apoptotic effect of Rela, we isolated primary chondrocytes from Prrx1-Cre;Relafl/fl and Relafl/fl mice, cultured them with or without 10 ng/mL TNF-α, and compared gene expression profiles by microarray analyses.

2016-09-15 | GSE79233 | GEO

The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

Project description:G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells. HaCaT cells were pre-treated with terbutaline or GW9508, TNF-alpha + IFN-gamma were then added, and cultured for another 24 h. Cells were then used for RNA extraction and hybridization on Affymetrix microarrays. We sought to clarify changes in gene expression after 1) TNF-alpha + IFN-gamma, 2) TNF-alpha + IFN-gamma + terbutaline, and 3) TNF-alpha + IFN-gamma + GW9508 treatment. To this end, we set 4 groups of samples; 1) unstimulated group, 2) TNF-alpha + IFN-gamma-stimulated group, 3) TNF-alpha + IFN-gamma + terbutaline-stimulated group, and 4) TNF-alpha + IFN-gamma + GW9508-stimulated group. In each group, HaCaT cells were stimulated in triplicate wells (n=3).

2010-12-01 | E-GEOD-20297 | biostudies-arrayexpress

Differential protein secretome induced by TNF-alpha

Project description:Endothelial-mesenchymal-transition (EndMT) is an important source of cancer-associated fibroblasts (CAFs), which are known to facilitate tumor progression. We have previously shown that EndMT is present in pancreatic tumors and that deficiency of the Tie1 receptor induces EndMT in human endothelial cells. Pancreatic tumors are characterized by the presence of tumor necrosis factor-α (TNF-α). We now show that TNF-α strongly induces human endothelial cells to undergo EndMT. In order to know the secretory feature of cells which undergo EndMT by TNF-α, we conducted a comparative analysis of HMVEC secretome treated or not for 24h and 48h with TNF-α. Secretome study shows that cells treated with TNF-α have an important fibroblast-like secretory capacity, and a proinflamatory signature. Moreover, Ingenuity Pathway Analysis (IPA) shows that pathways implicated in migration, inflammation and fibrosis are predicted to be activated and that necrosis and apoptosis pathways are inhibited. Accordingly cell survival, viability and cycle progression are activated. We show that TNF-α- treated cells secrete proteins related to 16 protumoral pathways, confirming their fibroblastic characteristic. Finally, among the predicted upstream regulators activated, IPA analysis shows that, TNFSF12 and its receptor are present at hight levels in PDAC patients. Altogether these results show the fibroblastic characteristic of treated cells and demonstrate that TNF-α induces CAFs.

2021-09-08 | PXD014488 | Pride

Transcription profiling of rat chondrocytes were treated with TNF-a with or without the MEK1/2 inhibitor U0126 for 24 h to investigate TNF-a-induced MEK/ERK-dependent regulation of Cartilage Matrix Genes

Project description:TNF-a is increased in the synovial fluid of patients with rheumatoid arthritis and osteoarthritis. TNF-a activates MEK/ERK in chondrocytes; however the overall functional relevance of MEK/ERK to TNF-a-regulated gene expression in chondrocytes is unknown. Chondrocytes were treated with TNF-a with or without the MEK1/2 inhibitor U0126 for 24 h. Microarray analysis was used to identify genes regulated by TNF-a in a MEK1/2-dependent fashion. Experiment Overall Design: Primary chondrocytes from the femoral condyles of neonatal rats were treated with DMSO (control sample), TNF-a, U0126 (selective MEK1/2 inhibitor) or TNF-a and U0126. Two biological replicates were collected for each treatment. Total RNA was collected and analyzed by Affymetrix Microarray.

2009-01-17 | E-GEOD-14402 | biostudies-arrayexpress

Osteoarthritic chondrocytes undergo a glycolysis-related metabolic switch upon exposure to IL-1β or TNF-α

Project description:Osteoarthritic chondrocytes undergo a glycolysis-related metabolic switch upon exposure to IL-1β or TNF-α

| PRJNA888116 | ENA

Mice VSMCs: Control vs. TNF-α cultured

Project description:Mice VSMCs: Control vs. TNF-α cultured

| PRJNA524301 | ENA

Gene expression analysis of TNF-alpha stimulated CaCo-2 cells

Project description:The series was designed to obtain gene expression patterns of TNF-alpha stimulated CaCo-2 cells. Keywords: TNF-alpha stimulation This series represents a group of 18 samples in 2 groups: 10 samples derived from not stimulated CaCo-2 cells, 8 samples from CaCo-2 cells stimulated with TNF-alpha in final concentration of 5 ng/ml for 60 min.

2010-06-25 | E-GEOD-10108 | biostudies-arrayexpress

Gene expression analysis of TNF-alpha stimulated THP-1 cells

Project description:The series was designed to obtain gene expression patterns of TNF-alpha stimulated THP-1 cells. Keywords: TNF-alpha stimulation This series represents a group of 15 samples in two groups: 7 samples derived from not stimulated THP-1 cells, 8 from THP-1 cells stimulated with TNF-alpha in a final concentration of 5 ng/ml for 60 min.

2010-06-25 | E-GEOD-10106 | biostudies-arrayexpress

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