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Genome-wide mRNA expression analysis of primary cultured mouse brain microvascular endothelial cells after inhibition of PKC-beta

ABSTRACT: Pharmacological inhibition of protein kinase C beta (PKC-beta) # by the compound LY317615 has been tested on primary cultured mouse brain microvascular endothelial cells, stimulated in-vitro for 8h at a concentration of 5 µM. The aim of the study was the question if inhibition of PKC-beta leads to inhibition of genes responsible for T-cell migration in order to investigate LY-317615 as a possible experimental therapy for multiple sclerosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE48572 | GEO | 2013/07/08

SECONDARY ACCESSION(S): PRJNA210721

REPOSITORIES: GEO

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Genome-wide mRNA expression analysis of primary cultured mouse brain microvascular endothelial cells after inhibition of PKC-beta

Project description:Pharmacological inhibition of protein kinase C beta (PKC-beta) # by the compound LY317615 has been tested on primary cultured mouse brain microvascular endothelial cells, stimulated in-vitro for 8h at a concentration of 5 ÂµM. The aim of the study was the question if inhibition of PKC-beta leads to inhibition of genes responsible for T-cell migration in order to investigate LY-317615 as a possible experimental therapy for multiple sclerosis. primary cultured mouse brain microvascular endothelial cells (MBMEC) have been prepared from new-born mice and cultured for one week. Then stimulated for 8h with 5 ÂµM LY317615. Two samples had been treated for the last 24h with 500 ÂµM TNF-alpha and 500 ÂµM IFN-gamma (inflamed) whereas two samples had been left untreated (naive). RNA was prepared using TRIZOL according to standard protocols.

2013-07-08 | E-GEOD-48572 | biostudies-arrayexpress

Effect of high or low chronic shear stress on microvascular endothelial cells cultured on native- versus AGE-fibronectin

Project description:Pulmonary microvascular endothelial cells were cultured on the inner surface of fibers (each 700 µm inner diameter) coated with either with native- or advanced glycation endproduct (AGE) modified fibronectin in hollow-fiber cartridges (FiberCell Systems, Inc.). Duration of shear stress application was 10 days. Shear stress was gradually increased to 17 dyne/cm2 in 2 samples (GSM32266: native fibronectin high shear stress or GSM45608: AGE-fibronectin) or was kept at constant low level of 1 dyne/cm2 in 1 sample (GSM41248: native fibronectin low shear stress). Keywords: parallel sample

2005-12-31 | E-GEOD-2424 | biostudies-arrayexpress

The role of PKC-beta in B cell activation

Project description:The role of PKC-beta in B cell activation

| PRJNA437924 | ENA

Effect of high or low chronic shear stress on microvascular endothelial cells cultured on native- versus AGE-fibronectin

2006-01-01 | GSE2424 | GEO

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.

2013-04-03 | GSE43217 | GEO

Targeting PKC: A Novel Role for beta-catenin in ER stress and Apoptotic Signaling

Project description:Targeting protein kinase C (PKC) isoforms by the small molecule inhibitor enzastaurin has shown promising pre-clinical activity in a wide range of tumor cells. In this study, we further delineated its mechanism of action in multiple myeloma (MM) cells and found a novel role of b-catenin in regulating growth and survival of tumor cells. Specifically, inhibition of PKC leads to rapid accumulation of b-catenin by preventing the phosphorylation required for its proteasomal degradation. Microarray analysis and siRNA-mediated gene silencing in MM cells revealed that accumulated b-catenin activates early ER stress signaling via eIF2a, CHOP and p21, leading to immediate growth inhibition. Furthermore, accumulated b-catenin contributes to enzastaurin-induced cell death. Both sequential knock-down of b-catenin, c-Jun, and p73, as well as overexpression of b-catenin or p73 confirmed that accumulated b-catenin triggers c-Jun-dependent induction of p73, thereby conferring MM cell apoptosis. In summary, our data reveal a novel role of b-catenin in ER stress-mediated growth inhibition, and a new pro-apoptotic mechanism triggered by b-catenin upon inhibition of PKC isoforms. Moreover, we identify p73 as a potential novel therapeutic target in MM. Based on these and previous data, enzastaurin is currently under clinical investigation in a variety of hematologic malignancies including MM. Keywords: time course

2008-11-11 | GSE13514 | GEO

Chromatinized PKC-q directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells

Project description:Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. Signal transduction kinases play a pivotal role as chromatin-anchored proteins in eukaryotes. Here we report for the first time that protein kinase C-theta (PKC-q) regulates EMT by acting as a critical chromatin-anchored switch for inducible genes via TGF-β and the key inflammatory regulatory protein, NFkB. Chromatinized PKC-q exists as an active transcription complex and is required to establish a permissive chromatin state at signature EMT genes. Genome-wide analysis identifies a unique cohort of inducible PKC-q-sensitive genes that are directly tethered to PKC-q in the mesenchymal state. Collectively, we show that crosstalk between signaling kinases and chromatin is critical for eliciting inducible transcriptional programs that drive mesenchymal differentiation and CSC formation, providing novel mechanisms to target using epigenetic therapy in breast cancer.

2014-06-22 | GSE53320 | GEO

Gene expression profiling in endothelial precursor cells of patients protected from microvascular complications

Project description:In this study, we examined the impact of modulating the TGF-β/PAI-1 axis in CD34+ cells function from diabetic patients and controls. Using gene array studies, we found that diabetics, protected from microvascular complications despite suboptimal glycemic control, had reduced level of TGF- β1 and PAI-1 transcripts in their CD34+ cells compared to age, sex, duration and degree of glycemic control -matched diabetics with microvascular complications. Treatment with neutralizing antibody to TGF- β1 in murine hematopoietic stem cells (HSC) enhanced in vivo repopulation potential of these cells in bone marrow transplantation; reduced the time required for cell division of single cells, increased survival of the progenitor cells and reduced TGF-β1 expression. TGF- β1 phosphorodiamidate morpholino oligomers (PMO) treatment reduced PAI-1 mRNA expression in diabetic (p<0.01) and non-diabetic (p=0.05) CD34+ cells. Inhibition of PAI-1 promoted CD34+ cell proliferation and migration in vitro.Targetting TGFβ-1/PAI-1 system offers a promising therapeutic strategy for restoring vascular reparative function in diabetic CD34+ cells and hematopoietic stem cells, enhancing key functions needed for cell therapy. Peripheral blood from either age matched controls (n=5), diabetics with long standing poorly controlled diabetes and no microvascular complications (n=4), and diabetics with long-standing poorly controlled diabetes with severe microvascular complications (n=5) was obtained and CD34+ cells were isolated. RNA was extracted followed by AffyNugen amplification, and the cDNA was probed to Human RSTA Affymetrix 2.0 chip

2013-02-01 | E-GEOD-43950 | biostudies-arrayexpress

Trancriptomic analysis of PKA and PKC signalling gene cascade in cultured human ovarian granulosa cells (KGN) [PMA treatments]

Project description:The oocyte’s capacity to complete maturation, to succeed fertilization and to reach the blastocyst stage is what defines the oocyte’s competence. The oocyte acquires this competence working closely with somatic cells of the follicle. Cumulus and granulosa cells provided support for the oocyte’s development and conversely the oocyte influence follicular cell growth and differentiation. Existing studies support the idea that follicular-stimulated hormone and luteinizing hormone play an essential role in oocyte competence acquisition through protein kinase A (PKA) and protein kinase C (PKC) signalling in granulosa cells. Therefore, human-like granulosa cells (KGN) were treated with forskolin 10 μM and phorbol 12-myristate 13-acetate 0.1 μM for 24 hours in order to process a transcriptomic analysis of differentially express genes between treatment. Over 2000 genes were founded to be differentially express at cut-off fold change of 1.5 and a p-value of 0.05. Five major upstreams, EGF, TGFB1, VEGF, FGF2 and HGF were founded to play an important role in competence acquisition thought PKA and PKC signalling. Differentially expressed targeted genes of both signalling pathways were classified in seven major ovarian functions such as PTGS2, IL8 and IL6 in inflammation, STAR, CYP11A1, CYP19A1 in steroidogenesis, VEGFC, VEGFA, CXCR4 in angiogenesis, AREG, EGFR, SPRY2 in differentiation, BAX, BCL2L12, CASP1 in apoptosis, CCND1, CCNB1, CCNB2 in division and MMP1, MMP9, TIMP1 in ovulation. Taken together, the results of this study suggest that PKA and PKC signalling potentiate their effects in some functions such as inflammation and apoptosis while some others are more specific to one or the other protein kinase like differentiation, ovulation and angiogenesis that are thought to be more PKC-dependent in human granulosa cells.

2016-07-20 | GSE84542 | GEO

Trancriptomic analysis of PKA and PKC signalling gene cascade in cultured human ovarian granulosa cells (KGN) [FSK treatments]

2016-07-20 | GSE84541 | GEO

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