Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Interfering with Proximal TLR4 to NF-kappaB Signal Transduction in Human Monocytes


ABSTRACT: This study investigated the global effect of carbon monoxide (CO) gas (250 ppm) on LPS- induced gene expression in THP-1 cells. CO predominantly suppresses LPS-induced gene response. Of the CO-suppressed genes, 18% were transcription factors and most others were cytokines, chemokines and immune response genes. Sequence analysis B binding siteskappafound that 81% of the gene promoters have putative NF- These results suggest that CO inhibits LPS-induced inflammatory B signaling pathwayresponse through regulating NF- The microarrays were performed on THP-1 cells, a human monocytic cell line. Cells were treated with or without LPS (1 ug/ml) in presence or absence of carbon monoxide (250 ppm) for 1 h. Total RNA was isolated, reverse transcribed, labeled and hybridized to oligonucleotide microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Peter Munson 

PROVIDER: E-GEOD-16193 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Carbon monoxide blocks lipopolysaccharide-induced gene expression by interfering with proximal TLR4 to NF-kappaB signal transduction in human monocytes.

Chhikara Maneesha M   Wang Shuibang S   Kern Steven J SJ   Ferreyra Gabriela A GA   Barb Jennifer J JJ   Munson Peter J PJ   Danner Robert L RL  

PloS one 20091202 12


Carbon monoxide (CO) is an endogenous messenger that suppresses inflammation, modulates apoptosis and promotes vascular remodeling. Here, microarrays were employed to globally characterize the CO (250 ppm) suppression of early (1 h) LPS-induced inflammation in human monocytic THP-1 cells. CO suppressed 79 of 101 immediate-early genes induced by LPS; 19% (15/79) were transcription factors and most others were cytokines, chemokines and immune response genes. The prototypic effects of CO on transcr  ...[more]

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