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Expression data from primary term human decidual cells treated with interleukin-1-beta for 6 hours.

ABSTRACT: Preterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58220 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA251636

REPOSITORIES: GEO

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Expression data from primary term human decidual cells treated with interleukin-1-beta for 6 hours.

Project description:Preterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge. Decidualized human endometrial stromal cells were treated with 1 ng/ml of interleukin-1-beta for 6 hours, while control cells were treated with 0.1% PBS containing 0.1% bovine serum albumin (vehicle). The cells were subjected to RNA extraction, quantification, and evaluation, followed by hybridization on Affymetrix Human Gene 2.0 ST Arrays (Platform GPL16686). Three biological replicates were used (6 total samples).

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Expression data from human amnion mesenchymal cells treated with interleukin-1-beta for 1hr and 8hr

Project description:Premature birth continues to be a challenging pregnancy complication, and a body of literature indicates that inflammation can contribute to premature delivery by converting a receptive uterine environment to a hostile one. Cytokines have been demonstrated to provoke up-regulation of inflammatory genes (e.g. interleukin-1, 6, and 8, tumor necrosis factor-alpha, cyclooxygenase-2, and microsomal prostaglandin E synthase-1). Using monolayer cultures of human amnion mesenchymal cells (AMCs) as a model, we aimed to detail the global programme of gene expression that occurs in response to cytokine challenge. Human amnion mesenchymal cells were challenged with 10 ng/ml of interleukin-1-beta for 1 hour (1h) or 8 hours (8h) in serum-free media, while control cells were treated with serum free medium only (veh). The cells (veh, 1h and 8h) were subjected to RNA extraction, quantification, and evaluation, followed by hybridization on Affymetrix GeneChip® Human Genome U133A 2.0 Arrays (Platform GPL571). Experiments were repeated three times for a total of nine samples used for microarray analysis. Three biological replicates were used to ensure that any results were not biased by day-to-day variation in RNA extraction.

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