Transcriptomics

Dataset Information

40

Effect of P. gingivalis on human primary gingival epithelial cells


ABSTRACT: EXPERIMENT: Microarray expression profiles derived from the human primary gingival epithelial cells 24.0h after exposure to heat inactivated P. gingivalis ANIMAL MODEL: NON EXPOSURE: Human primary gingival epithelial cells (at 3rd passage) were exposed to heat inactivated P. gingivalis (MOI:100) at 90% confluence. Two types of gingival epithelial cells were used. One with Normal cytokine inducer type (at least 2 fold IL-6/TNF-alpha/IL-1ß when challenged with TLR2/4 agonists) and the other with diminished cytokine inducer type (no change in IL-6/TNF-alpha/IL-1ß when challenged with TLR2/4 agonists). INTERVAL: NON. PLATFORM: microRNA expression profile in gingival epithelial cells - miRCURY LNA™ microRNA Arrays (Exiqon). The RNA samples were subjected to microarray on 8/9/2007 Keywords = Human primary gingival epithelial cells Keywords = P. gingivalis Keywords = Periodontitis Keywords: Ordered The effect of heat inactivated P. gingivalison human primary gingival epithelial cells were assayed.

ORGANISM(S): Homo sapiens  

SUBMITTER: Manjunatha R Benakanakere  Denis F Kinane   Amar Singh   Amar V Singh    

PROVIDER: E-GEOD-13042 | ArrayExpress | 2014-05-04

SECONDARY ACCESSION(S): GSE13042PRJNA109951

REPOSITORIES: GEO, ArrayExpress

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Publications

Modulation of TLR2 protein expression by miR-105 in human oral keratinocytes.

Benakanakere Manjunatha R MR   Li Qiyan Q   Eskan Mehmet A MA   Singh Amar V AV   Zhao Jiawei J   Galicia Johnah C JC   Stathopoulou Panagiota P   Knudsen Thomas B TB   Kinane Denis F DF  

The Journal of biological chemistry 20090609 34


Mammalian biological processes such as inflammation, involve regulation of hundreds of genes controlling onset and termination. MicroRNAs (miRNAs) can translationally repress target mRNAs and regulate innate immune responses. Our model system comprised primary human keratinocytes, which exhibited robust differences in inflammatory cytokine production (interleukin-6 and tumor necrosis factor-alpha) following specific Toll-like receptor 2 and 4 (TLR-2/TLR-4) agonist challenge. We challenged these  ...[more]

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