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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.

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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

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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.

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

2016-07-20 | GSE84541 | GEO