Transcriptional profiling of oral keratinocytes was utilized to define the biological role of P. gingivalis SerB.
Role of Porphyromonas gingivalis SerB in gingival epithelial cell cytoskeletal remodeling and cytokine production.
No sample metadata fields
View SamplesTranscriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by co-culture with the oral commensal S. gordonii and the opportunistic commensal F. nucleatum.
Gingival epithelial cell transcriptional responses to commensal and opportunistic oral microbial species.
No sample metadata fields
View SamplesWe investigated the association between subgingival bacterial profiles and gene expression patterns in gingival tissues of patients with periodontitis.
Subgingival bacterial colonization profiles correlate with gingival tissue gene expression.
Specimen part
View SamplesWe examined gene expression signatures in healthy and diseased gingival tissues in 90 patients. Analysis of the gingival tissue transcriptome in states of periodontal health and disease may reveal novel insights of the pathobiology of periodontitis.
Transcriptomes in healthy and diseased gingival tissues.
Specimen part
View SamplesTranscriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by mono- and complex co-culture with oral commensal S. gordonii and pathogenic P. gingivalis.
The degree of microbiome complexity influences the epithelial response to infection.
No sample metadata fields
View SamplesTranscriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by co-culture with the oral pathogenic Porphyromonas gingivalis and Aggregatibacter (formerly actinobacillus) actinomycetemcomitans.
Distinct transcriptional profiles characterize oral epithelium-microbiota interactions.
No sample metadata fields
View SamplesTranscriptional profiling of a DEX-inducible SNRK3.15 seedlings in the presence of ABA.
A mesoscale abscisic acid hormone interactome reveals a dynamic signaling landscape in Arabidopsis.
None
Age, Time
View SamplesThe objectives of this investigation were to examine changes in the host transcriptional profiles during a Porphyromonas gingivalis infection using a murine calvarial model of inflammation and bone resorption. P. gingivalis strain 381 was injected into the subcutaneous soft tissue over the calvaria of BALB/c mice for 3 days, after which the soft tissues and calvarial bones were excised. RNA was isolated from infected soft tissues and calvarial bones and analyzed for transcript profiles using Murine GeneChip MG-MOE430A Affymetrix arrays to provide a molecular profile of the events that occur following infection of these tissues.
Porphyromonas gingivalis infection-induced tissue and bone transcriptional profiles.
Age, Specimen part
View SamplesWe report the effect of DKK1 treatment during culture on the length and transcriptome of embryos on day 15 of development, supporting the notion that changes early in development affect later stages of development. Overall design: Bovine embryos were produced in vitro and exposed to either 0 or 100 ng/ml DKK1 from day 5 to 7 of culture. Embryos were transferred on day 7 and recovered on day 15 for evaluation of length and transciptome
Dickkopf-related protein 1 is a progestomedin acting on the bovine embryo during the morula-to-blastocyst transition to program trophoblast elongation.
Treatment, Subject
View SamplesBackground & Aims: Ursodeoxycholic acid (UDCA) attenuates chemical and colitis-induced colon carcinogenesis in animal models. We investigated its mechanism of action on normal intestinal cells, in which carcinogenesis- or inflammation-related alterations do not interfere with the result. Methods: Alterations of gene expression were identified in Affymetrix arrays in isolated colon epithelium of mice fed with a diet containing 0.4% UDCA and were confirmed in the normal rat intestinal cell line IEC-6 by RT-PCR. The effect of the insulin receptor substrate 1 (Irs-1) expression and of ERK phosphorylation on proliferation was investigated in vitro by flow cytometry, western blotting, siRNA-mediated gene suppression or by pharmacological inhibition of the kinase activity. The ERK1-effect on Irs-1 transcription was tested in a reporter system. Results: UDCA-treatment in vivo suppressed potential pro-proliferatory genes including Irs-1 and reduced cell proliferation by more than 30%. In vitro it neutralised the proliferatory signals of IGF-1 and EGF and slowed down the cell cycle. Irs-1 transcription was suppressed due to high ERK1 activation. Both Irs-1 suppression and the persistent high ERK activation inhibited proliferation. Conversely, the decrease of phosphorylation of ERK1 (but not ERK2) or of its expression partially abrogated the inhibitory effects of UDCA. Conclusions: UDCA inhibits proliferation of intestinal epithelial cells by acting upon IGF-1 and EGF pathways and targeting ERK1 and, consequently, Irs-1. The inhibition of these pathways adds a new dimension to the physiological and therapeutic action of UDCA and, since both pathways are activated in inflammation and cancer, suggests new applications of UDCA in chemoprevention and chemotherapy.
UDCA slows down intestinal cell proliferation by inducing high and sustained ERK phosphorylation.
Specimen part, Cell line
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