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Transcriptome profiling of gingival epithelial cells response to IRF1 silencing using RNA-seq

ABSTRACT: Transcriptome profiling of gingival epithelial cells response to IRF1 silencing using RNA-seq

PROVIDER: PRJNA764715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15974952.fastq.gz	Fastqsanger.gz
	SRR15974953.fastq.gz	Fastqsanger.gz
	SRR15974954.fastq.gz	Fastqsanger.gz
	SRR15974955.fastq.gz	Fastqsanger.gz
	SRR15974956.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of gingival epithelial cells response to IRF1 silencing using RNA-seq

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Project description: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-1Ã when challenged with TLR2/4 agonists) and the other with diminished cytokine inducer type (no change in IL-6/TNF-alpha/IL-1Ã when challenged with TLR2/4 agonists). INTERVAL: NON. PLATFORM: microRNA expression profile in gingival epithelial cells - miRCURY LNAâ¢ 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.

2010-05-16 | E-GEOD-13042 | biostudies-arrayexpress

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Project description: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

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Project description:In order to explain the molecular mechanisms of capsaicin-induced proliferation of gingival epithelial cells (GECs), a microarray analysis was performed. Several cell proliferation related genes were significantly up-regulated. These data suggest that TRPV1 signaling in GEC may induce transcriptional upregulation of growth factors, which results in an increased proliferation rate. Simian virus 40 (SV40) T-antigen-immortalized human gingival epithelial cell line, epi4, were stimulated with 1 M-NM-<M capsaicin for 4 hours. Total RNA was isolated and subjected to gene expression analysis using Agilent whole human genome oligo microarray.

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Transcriptome profiling of gingival epithelial cells response to IFN stimulation using RNA-seq

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Project description:Porphyromonas gingivalis is a pathogen in severe periodontal disease. Able to exploit an intracellular lifestyle within primary gingival epithelial cells (GECs), a reservoir of P. gingivalis can persist within the gingival epithelia. This process is facilitated by manipulation of the host cell signal transduction cascades which can impact cell cycle, cell death and cytokine responses. Using microarrays, we investigated the ability of P. gingivalis 33277 to regulate microRNA (miRNA) expression in GECs. One of several miRNAs differentially regulated by GECs in the presence of P. gingivalis was miR-203, which was upregulated 4-fold compared with uninfected controls. Differential regulation of miR-203 was confirmed by qRT-PCR. Putative targets of miR-203, suppressors of cytokine signaling (SOCS) 3 and 6, were evaluated by qRT-PCR. SOCS3 and SOCS6 mRNA levels were reduced >5-fold and >2-fold, respectively, in P. gingivalis-infected GECs compared with controls. Silencing miR-203 using a si-RNA construct reversed the inhibition of SOCS3 expression. A dual luciferase assay confirmed binding of miR-203 to the putative target binding site of SOCS3 3’ UTR. Western blot analysis demonstrated that activation of Stat3, a downstream target of SOCS, was diminished following miR-203 silencing. This study shows that induction of miRNAs by P. gingivalis can modulate important host signaling responses.

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The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

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