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E-GEOD-19772 - Expression Data From HCMV-Infected Human Monocytes 48 Hours Post-Infection: Role of PI(3)K
Released on 6 January 2010, last updated on 10 June 2011
Human cytomegalovirus (HCMV) induces pro-inflammatory monocytes following infection and we have evidence that phosphatidylinositol 3-kinase [PI(3)K] is a key mediator in this activation. To begin to address how this signalling pathway is responsible for the functional changes in infected monocytes, we examined the role this pathway played in the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of genes were regulated in a PI(3)K-dependent manner, identifying this pathway as a key cellular control point in the conversion of monocytes to an activated pro-inflammatory state following HCMV infection. Keywords: Disease state To begin to globally define how PI(3)K is involved in the HCMV-induced changes in monocyte function, we performed a transcriptome analysis in the presence of an inhibitor to the PI(3)K signalling pathway. Specifically, a cDNA microarray containing 12,626 unique probe sets was utilized to assess the modulation of the monocyte transcriptome at 48 hours post-infection in the presence of the pharmacological agent LY294002 (LY), a PI(3)K inhibitor. A total of 2 replicates from HCMV-infected monocytes, 2 replicates from LY-pretreated infected monocytes, and 2 replicates from mock-infected monocytes were analyzed in this study.
transcription profiling by array
Andrew D. Yurochko <email@example.com>, Andrew D Yurochko, Elizabeth R Bivins-Smith, M S Smith