Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in tracheal epithelial RTEC11 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Tracheal epithelial RTEC11 cells used in this study were derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Keywords: rat tracheal epithelial RTEC11; growth arrest; differentiation; gene expression
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in tracheal epithelial RTEC11 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Tracheal epithelial RTEC11 cells used in this study were derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Experiment Overall Design: A rat conditionally immortalized tracheal epithelial cell line, RTEC11, derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen was used. RTEC11 cells were cultured at permissive (33°C) or nonpermissive (39°C) temperature for 3 days.
Project description:Inflammation is a key component of pathological angiogenesis. Here we induce cornea neovascularisation using sutures placed into the cornea, and sutures are removed to induce a regression phase. We used whole transcriptome microarray to monitor gene expression profies of several genes
Project description:A series of two color gene expression profiles obtained using Agilent 44K expression microarrays was used to examine sex-dependent and growth hormone-dependent differences in gene expression in rat liver. This series is comprised of pools of RNA prepared from untreated male and female rat liver, hypophysectomized (‘Hypox’) male and female rat liver, and from livers of Hypox male rats treated with either a single injection of growth hormone and then killed 30, 60, or 90 min later, or from livers of Hypox male rats treated with two growth hormone injections spaced 3 or 4 hr apart and killed 30 min after the second injection. The pools were paired to generate the following 6 direct microarray comparisons: 1) untreated male liver vs. untreated female liver; 2) Hypox male liver vs. untreated male liver; 3) Hypox female liver vs. untreated female liver; 4) Hypox male liver vs. Hypox female liver; 5) Hypox male liver + 1 growth hormone injection vs. Hypox male liver; and 6) Hypox male liver + 2 growth hormone injections vs. Hypox male liver. A comparison of untreated male liver and untreated female liver liver gene expression profiles showed that of the genes that showed significant expression differences in at least one of the 6 data sets, 25% were sex-specific. Moreover, sex specificity was lost for 88% of the male-specific genes and 94% of the female-specific genes following hypophysectomy. 25-31% of the sex-specific genes whose expression is altered by hypophysectomy responded to short-term growth hormone treatment in hypox male liver. 18-19% of the sex-specific genes whose expression decreased following hypophysectomy were up-regulated after either one or two growth hormone injections. Finally, growth hormone suppressed 24-36% of the sex-specific genes whose expression was up-regulated following hypophysectomy, indicating that growth hormone acts via both positive and negative regulatory mechanisms to establish and maintain the sex specificity of liver gene expression. For full details, see V. Wauthier and D.J. Waxman, Molecular Endocrinology (2008)
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in astrocyte RCG-12 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Astrocyte RCG-12 cells used in this study were derived from primary cultured rat cortical glia cells infecting with a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Of the 15,923 probe sets analyzed, nonpermissive temperature differentially expressed 556 probe sets by >2.0-fold. Keywords: Astrocyte cell; growth arrest; differentiation; temperature-sensitive simian virus 40 large T-antigen; nonpermissive temperature