Gene induction by Dex, IL-9 and CCL-1 in BW5147 mouse T cell lymphoma. Mus musculus

The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology. Keywords: cytokine and dexamethasone stimulation Overall design: One million BW5147 cells were stimulated with 100 ng/ml of dexamethasone and/or with 100 U/ml of IL-9 or CCL1 for eight hours. RNA was then extracted for hybridization on Affymetrix microarrays. This experiment was performed in duplicates .

本研究旨在明确参与白细胞介素9（IL-9）和C-C趋化因子配体1（CCL1）介导的抗糖皮质激素诱导细胞凋亡的基因及作用机制。我们提出如下假说：真正关键的调控介质的表达，可分别被地塞米松（Dexamethasone, Dex）以及IL-9、CCL1这类抗凋亡细胞因子反向调控。为此，我们依托Affymetrix微阵列（Affymetrix microarray）技术，对经或未经地塞米松、IL-9及CCL1刺激的BW5147细胞的表达基因开展了全面分析。
关键词：细胞因子与地塞米松刺激
实验设计：将1×10⁶个BW5147细胞以100 ng/ml地塞米松、100 U/ml IL-9或CCL1单独或联合刺激8小时。随后提取RNA用于Affymetrix微阵列杂交。本实验以双重复形式开展。