Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA130311 | ENA |
REPOSITORIES: ENA
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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)
2008-05-24 | GSE11529 | GEO
Project description:Short-term in vitro culture of rat fetal testes with all-trans retinoic acid
| PRJNA395040 | ENA
Project description:The effects of retinoic acid/vitamin A signal on the transcriptional profile of the ductus arteriosus during development were examined. Keywords: time course, development, response to a nutritional agent
2007-09-30 | GSE3420 | GEO
Project description:Antimicrobial proteins form an essential chemical barrier that protects the intestinal epithelium from microbial invasion. REG3 family antimicrobial lectins are prominently induced by the microbiota, but how nutritional cues intersect with microbial signals to regulate their expression is poorly understood. Vitamin A plays a central role in mucosal adaptive immunity, but its contribution to epithelial innate immunity is unclear. Here, we show that dietary vitamin A promotes expression of REG3 antimicrobial lectins, including REG3G, in intestinal epithelial cells from both mice and humans. Vitamin A–dependent induction of REG3G expression is driven by retinoic acid and requires signaling through retinoic acid receptors (RARs). Mechanistically, RARs directly bind the Reg3g promoter adjacent to a binding site for STAT3, the transcription factor that transduces microbial signals, thereby integrating nutritional and microbial inputs at the level of REG3G transcription. Extending these findings, we demonstrate that vitamin A–retinoic acid signaling similarly promotes expression of α-defensin antimicrobial proteins. Together, these results define a transcriptional mechanism by which vitamin A enhances epithelial antimicrobial defenses to strengthen mucosal innate immunity.
2026-03-08 | GSE318054 | GEO
Project description:Organ - specific expression profiles of rat treated with targretin, 9-cis retinoic acid, and 4-hydroxyphenylretinamide
| PRJNA94205 | ENA
Project description:In order to establish a rat embryonic stem cell transcriptome, mRNA from rESC cell line DAc8, the first male germline competent rat ESC line to be described and the first to be used to generate a knockout rat model was characterized using RNA sequencing (RNA-seq) analysis.
2016-09-02 | GSE44150 | GEO
Project description:Vitamin A (retinol) is an essential precursor for the production of retinoic acid (RA), which in turn is a major regulator of gene expression, affecting cell differentiation throughout the body. Understanding how vitamin A nutritional status, as well as therapeutic retinoid treatment, regulates the expression of retinoid homeostatic genes is important for improving dietary recommendations and therapeutic strategies using retinoids. This study investigated genes central to processes of retinoid uptake and storage, release to plasma, and oxidation in the liver of rats under steady-state conditions after different exposures to dietary vitamin A (deficient, marginal, adequate and supplemented), and acutely after administration of a therapeutic dose of all-trans-RA. Over a very wide range of dietary vitamin A, lecithin:retinol acyltransferase (LRAT) as well as multiple cytochrome P450s (CYP26A1, CYP26B1, and CYP2C22) differed by diet and were highly correlated with one another and with vitamin A status assessed by liver retinol concentration (all correlations, P<0.05). After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding RARß, a classical direct target of RA. CYP26A1 mRNA exhibited the greatest dynamic range (change of log26 in 3 h). Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naïve rats. By in situ hybridization, CYP26A1 mRNA was strongly regulated within hepatocytes, closely resembling RBP4 in location. Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change.
2011-09-01 | GSE24104 | GEO