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

ABSTRACT: 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 NFκB and TNF-α, 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44747 | GEO | 2013/05/27

SECONDARY ACCESSION(S): PRJNA191531

REPOSITORIES: GEO

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Project description:The oocyteâs capacity to complete maturation, to succeed fertilization and to reach the blastocyst stage is what defines the oocyteâs competence. The oocyte acquires this competence working closely with somatic cells of the follicle. Cumulus and granulosa cells provided support for the oocyteâs 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 Î¼M and phorbol 12-myristate 13-acetate 0.1 Î¼M 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. 8 samples were analysed, 4 controls compared to 4 Phorbol 12-myristate 13-acetate treatments (total of 4 replicates).

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

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