PKC Activation Induces Inflammatory Response and Cell Death in Human Bronchial Epithelial Cells
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{"title"=>"PKC Activation Induces Inflammatory Response and Cell Death in Human Bronchial Epithelial Cells", "type"=>"journal", "authors"=>[{"first_name"=>"Hyunhee", "last_name"=>"Kim"}, {"first_name"=>"Ricardo", "last_name"=>"Zamel"}, {"first_name"=>"Xiao-Hui", "last_name"=>"Bai"}, {"first_name"=>"Mingyao", "last_name"=>"Liu"}], "year"=>2013, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"1932-6203", "pmid"=>"23691166", "doi"=>"10.1371/journal.pone.0064182"}, "id"=>"915e38fd-0a73-3b72-912d-4a0022362fb8", "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 of the respiratory system. We hypothesized that the activation of protein kinase C (PKC) is one of the essential mechanisms of inflammatory response in airway epithelial cells. In the present study, we stimulated human bronchial lung epithelial (BEAS-2B) cells with the phorbol ester Phorbol 12, 13-dibutyrate (PDBu), and examined gene expression profile using microarrays. Microarray analysis suggests that PKC activation induced dramatic changes in gene expression related to multiple cellular functions. The top two interaction networks generated from these changes 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 an 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-classes of PKC isozymes. We conclude that pathological cell death and cytokine production in airway epithelial cells in various situations may be mediated through PKC related signaling pathways. These findings suggest that PKCs can be new targets for treatment of lung diseases.", "link"=>"http://www.mendeley.com/research/pkc-activation-induces-inflammatory-response-cell-death-human-bronchial-epithelial-cells-2", "reader_count"=>5, "reader_count_by_academic_status"=>{"Student > Doctoral Student"=>2, "Researcher"=>2, "Student > Master"=>1}, "reader_count_by_user_role"=>{"Student > Doctoral Student"=>2, "Researcher"=>2, "Student > Master"=>1}, "reader_count_by_subject_area"=>{"Biochemistry, Genetics and Molecular Biology"=>3, "Neuroscience"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1}, "reader_count_by_subdiscipline"=>{"Neuroscience"=>{"Neuroscience"=>1}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>3}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"United States"=>1}, "group_count"=>0}

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  • {"files"=>["https://ndownloader.figshare.com/files/1063411", "https://ndownloader.figshare.com/files/1063412"], "description"=>"<div><p>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 of the respiratory system. We hypothesized that the activation of protein kinase C (PKC) is one of the essential mechanisms of inflammatory response in airway epithelial cells. In the present study, we stimulated human bronchial lung epithelial (BEAS-2B) cells with the phorbol ester Phorbol 12, 13-dibutyrate (PDBu), and examined gene expression profile using microarrays. Microarray analysis suggests that PKC activation induced dramatic changes in gene expression related to multiple cellular functions. The top two interaction networks generated from these changes 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 an 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-classes of PKC isozymes. We conclude that pathological cell death and cytokine production in airway epithelial cells in various situations may be mediated through PKC related signaling pathways. These findings suggest that PKCs can be new targets for treatment of lung diseases.</p> </div>", "links"=>[], "tags"=>["Anatomy and physiology", "Immune physiology", "cytokines", "genomics", "Functional genomics", "immunology", "Immune system", "immunity", "inflammation", "Molecular cell biology", "Signal transduction", "Signaling cascades", "Protein kinase signaling cascade", "Signaling in cellular processes", "Protein kinase C signaling", "Cell death", "Pulmonology", "activation", "inflammatory", "bronchial", "epithelial"], "article_id"=>704678, "categories"=>["Medicine", "Biological Sciences"], "users"=>["Hyunhee Kim", "Ricardo Zamel", "Xiao-hui Bai", "Mingyao Liu"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0064182.s001", "https://dx.doi.org/10.1371/journal.pone.0064182.s002"], "stats"=>{"downloads"=>1, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_PKC_Activation_Induces_Inflammatory_Response_and_Cell_Death_in_Human_Bronchial_Epithelial_Cells_/704678", "title"=>"PKC Activation Induces Inflammatory Response and Cell Death in Human Bronchial Epithelial Cells", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2013-05-17 01:17:58"}

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Relative Metric

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