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Gene expression profile changes in PKC-inhibitor-pretreated HT1080 cells cells after TLR3 stimulation

ABSTRACT: TLR3 stimulation by extracellular dsRNA (e.g. polyIC) induces expression of numerous genes. The inhibition of PKC by Go6976 prior to TLR3 stimulation leads to an ablation of expression of IRF-3-dependent genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43217 | GEO | 2013/04/03

SECONDARY ACCESSION(S): PRJNA184996

REPOSITORIES: GEO

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Gene expression profile changes in PKC-inhibitor-pretreated HT1080 cells cells after TLR3 stimulation

Project description:TLR3 stimulation by extracellular dsRNA (e.g. polyIC) induces expression of numerous genes. The inhibition of PKC by Go6976 prior to TLR3 stimulation leads to an ablation of expression of IRF-3-dependent genes. Total RNA extracted from HT1080 cells with or without 1 h pretreatment with 5 uM Go6976, after 6 h of treatment with dsRNA (polyIC), compared to untreated controls

2013-04-03 | E-GEOD-43217 | biostudies-arrayexpress

Gene expression profile changes in HDAC6 knockdown HT1080 cells cells after TLR3 stimulation

Project description:TLR3 stimulation by extracellular dsRNA (e.g. polyIC) induces expression of numerous genes. The knockdown of HDAC6 prior to TLR3 stimulation leads to an ablation of expression of IRF-3-dependent genes. Total RNA extracted from HT1080 cells expressing control-shRNA or HDAC6-shRNA, after 6 h of treatment with dsRNA (polyIC), compared to untreated controls

2013-12-31 | E-GEOD-43218 | biostudies-arrayexpress

Gene expression profile changes in HDAC6 knockdown HT1080 cells cells after TLR3 stimulation

2013-12-31 | GSE43218 | GEO

Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

Project description:we assessed the impact of TLR3 L412F at endogenous cellular levels upon double stranded RNA (dsRNA) stimulation, by performing RNA-sequencing in primary fibroblasts from individuals homozygous for the ancestral allele (n =2) or homozygous for TLR3 L412F (n = 4) upon extracellular Poly(I:C) stimulation that activates the TLR3 pathway. The average response of TLR3 L412F homozygotes was significantly decreased (mean Δ log2 fold-change = 0.93; Wilcoxon p <10-16) compared to that of cells with the ancestral allele, approaching that of TLR3-deficient cells, used as negative control.

2023-01-13 | GSE216304 | GEO

Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs) Fibroblast cells and PBMCs from donors with autosomal recessive (AR) complete TLR3 deficiency and autosomal dominant (AD) partial TLR3 deficiency were collected for microarray analysis to measure the transcriptional responsiveness of TLR3 in fibroblast and PBMCs. A total of 3 healthy controls, 1 AD TLR3-deficient patient, 1 AR TLR3-deficient patient, 1 AR UNC-93B-deficient patient, 1 MyD88 deficient patien were used in this study. The fibroblast cells were cultured in DMEM medium supplemented with 10% fetal calf serum (FCS). The PBMCs were cultured in RPMI medium complemented with 10% FCS. Different kinetics (2 hours and 8 hours) of poly(I:C) (25ug/ml, purchased from Amersham) stimulations were performed, aiming to define TLR3-inducible genes in these human cells. A stimulation of IL-1β (20ng/ml, purchased from R&D system Inc.) was used as a positive activation control with same kinetics of stimulations. A total of one million cells per stimulation were used for fibroblasts, and around 1.5 million cells per stimulation for PBMCs.

2011-11-02 | E-GEOD-30951 | biostudies-arrayexpress

TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors

2011-03-02 | GSE27579 | GEO

TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors DRGN were cultures 5 days prior to a 16 hour stimulation - Three separate studies were analyzed for inflammatory response

2011-03-02 | E-GEOD-27579 | biostudies-arrayexpress

The hTERT-RPE1 secretome after TLR3 stimulation

Project description:RPE cells perform a number of support functions in the inner eye including the secretion of signalling molecules and the maintenance of the immune privileged environment through communication with the immune system (Detrick and Hooks, 2010). Previous reports have demonstrated that RPE cells express a number of TLRs including the viral RNA receptor TLR3. To determine the complete secretory response of RPE cells downstream of poly(I:C) stimulation, we analysed conditioned medium from unstimulated or poly(I:C)-stimulated RPE cells using quantitative SILAC mass spectrometry.

2020-06-16 | PXD019445 | Pride

Noncoding dsRNA induces retinoic acid synthesis to stimulate hair follicle regeneration via TLR3

Project description:This SuperSeries is composed of the SubSeries listed below. How developmental programs reactivate in regeneration is a fundamental question in biology. We addressed this question through the study of Wound Induced Hair follicle Neogenesis (WIHN), an adult organogenesis model where stem cells regenerate de novo hair follicles following deep wounding. The exact mechanism is uncertain. Here we show that self-noncoding dsRNA activates the anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice. Additionally, in humans, rejuvenation lasers induce gene expression signatures for dsRNA and RA, with measurable increases in intrinsic RA synthesis. These results demonstrate a potent stimulus for RA synthesis by non-coding dsRNA, relevant to their broad functions in development and immunity.

2019-05-22 | GSE128868 | GEO

PKC Activation Induces Inflammatory Response and Cell Death in Human Bronchial Epithelial Cells

Project description:A variety of airborne pathogens can induce inflammatory responses in airway epithelial cells, which is a crucial component of host defence. However, excessive inflammatory responses and chronic inflammation also contribute to different diseases in the respiratory system. We hypothesized that the activation of protein kinase C (PKC) is one of the essential mechanisms of inflammatory responses in airway epithelial cells. In the present study, we stimulated human bronchial lung epithelial (BEAS-2B) cells with phorbol ester Phorbol 12, 13-dibutyrate (PDBu), and examined gene expression profile with microarray analysis. Bioinformatics suggested that PKC activation induced dramatic changes in gene expression related to multiple cellular functions. The top two functional networks of genes were centered on NFM-NM-:B and TNF-M-NM-1, which are two commonly known pathways for cell death and inflammation. Subsequent tests confirmed the decrease in cell viability and increase in the production of various cytokines. Interestingly, each of the increased cytokines was differentially regulated at mRNA and/or protein levels by different sub-class of PKC isozymes. We conclude that many pathogen-induced cell death and cytokine production in airway epithelial cells may be mediated through PKC related signaling pathways. These findings suggest that PKCs can be new targets for treatments of lung diseases. Three groups of BEAS-2B cells were prepared: control, 0.5 hour of PDBu stimulation, and 4 hours of PDBu stimulation. Each group consisted of three biological replicates.

2013-05-27 | E-GEOD-44747 | biostudies-arrayexpress

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