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Transcription profiling time series of cultured human keratinocytes treated with TNFalpha in the presence or absence of the NFkB inhibitor parthenolide

ABSTRACT: Cultured keratinocytes treated with TNFa in the presence or absence of NFkB inhibitor; time course 1, 4, 24 & 48 hrs.

ORGANISM(S): Homo sapiens

SUBMITTER: Miki Blumenberg

PROVIDER: E-GEOD-2489 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Pathway-specific profiling identifies the NF-kappa B-dependent tumor necrosis factor alpha-regulated genes in epidermal keratinocytes.

Banno Tomohiro T Gazel Alix A Blumenberg Miroslav M

The Journal of biological chemistry 20050218 19

Identification of tumor necrosis factor alpha (TNF alpha) as the key agent in inflammatory disorders led to new therapies specifically targeting TNF alpha and avoiding many side effects of earlier anti-inflammatory drugs. However, because of the wide spectrum of systems affected by TNF alpha, drugs targeting TNF alpha have a potential risk of delaying wound healing, secondary infections, and cancer. Indeed, increased risks of tuberculosis and carcinogenesis have been reported as side effects aft ...[more]

PMID: 15722350

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TNF & Parthenolide treatment of keratinocytes

Project description:Cultured keratinocytes treated with TNFa in the presence or absence of NFkB inhibitor; time course 1, 4, 24 & 48 hrs. Keywords = Epidermis Keywords = skin Keywords = keratinocytes Keywords = inflammation Keywords = NFkB Keywords = TNFa Keywords: time-course

2005-04-06 | GSE2489 | GEO

Transcription profiling of human epidermal keratinocytes treated with IL-1

Project description:Interleukin-1 is a proinflammatory and immunomodulatory cytokine that plays a crucial role in inflammatory diseases of the skin, including bacterial infections, bullous diseases, UV damage and especially psoriasis. To characterize the molecular effects of IL-1 in epidermis, we defined the transcriptional changes in human epidermal keratinocytes 1, 4, 24, and 48 h after treatment with IL-1a. IL-1 significantly regulated 388 genes, including genes associated with proteolysis, adhesion, signal transduction, proliferation, and epidermal differentiation. IL-1 induces many genes that have antimicrobial function. Secreted cytokines, chemokines, growth factors, and their receptors are the prominent targets of IL-1 regulation, including IL-8, IL-19, elafin, C3, and S100A proteins, which implicates IL-1 in the pathogenesis of inflammatory diseases. IL-1 induced not only proliferation-associated genes but also differentiation marker genes such as transglutaminase-1 and involucrin, which suggests that IL-1 plays an important role in the aberrant proliferation and differentiation seen in psoriasis. Correlation of IL-1 regulated genes with the TNFa and IFNg regulated ones showed more similarities between IL-1 and TNFa than IL-1 and IFNg, whereas Oncostatin-M affected a largely unrelated set of genes. IL-1 regulates many genes previously shown to be specifically over-expressed in psoriasis. In summary, IL-1 regulates a characteristic set of genes that define its specific contribution to inflammation and aberrant differentiation in skin diseases. Experiment Overall Design: keratinocytes were treated with 25 ng/ml IL-1 and transcriptomes compared to untreated controls at 1, 4, 24 and 48 h post treatment.

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Transcription profiling of human epidermal keratinocytes treated with IFN-gamma reveals IFN-gamma suppressed the expression of over 100 genes responsible for cell cycle, DNA replication and RNA metabolism.

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A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 2)

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A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 2)

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