Keratinocytes in embryos and newborns, and Notch1 expression in newborns
Ontology highlight
ABSTRACT: Comparison between pattern of gene expression in uncultured keratinocytes derived from the epidermis of embryonic mice (E15.5) versus newborn mice and comparison between pattern of gene expression in primary keratinocytes derived from newborn mice plus/minus activated Notch1 expression. Keywords = mouse Keywords = keratinocyte Keywords = skin Keywords = embryonic development. Keywords: other
Project description:Comparison between pattern of gene expression in uncultured keratinocytes derived from the epidermis of embryonic mice (E15.5) versus newborn mice and comparison between pattern of gene expression in primary keratinocytes derived from newborn mice plus/minus activated Notch1 expression.
Project description:Microarray analysis of normal newborn ovarian transcript levels, for use in comparison to array based studies of differential expression in mouse knockout models. Experiment Overall Design: Newborn ovaries were pooled separately from wild type animals and total RNA isolated using RNeasy mini kit (Qiagen, CA). Newborn ovaries were collected within 12 hours of delivery. Animal experimentation was approved by the Institutional Animal Care and Use Committee of Baylor College of Medicine. Three independently pooled RNA samples from wild type used to generate biotinylated cRNA. Biotinylated cRNA was hybridized to GeneChip Mouse Expression Set 430 2.0 (Affymetrix, Inc.). Since three independent experiments were performed from three independent pools of wild type RNA, signal intensities for particular genes were averaged between the three chips.
Project description:We analyzed Brg1 binding genomeiwide in freshly isolated newborn mouse epidermal keratinocytes using ChIP-seq technology Mouse epidermal keratinocytes were isolated form the newborn C57Bl6 mice and Brg1 binding in their chromatin was analyzed using ChIP-seq technology on Hi-Seq 2500 machine
Project description:As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/). We compared the gene expression profiles of uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ (KO), Prdm16LacZ/+(HET), and Prdm16+/+ (WT) mice. The uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ, Prdm16LacZ/+, and Prdm16+/+ mice were dissected from the brains and placed into the Trizol reagent. Purified RNA was reverse transcribed and amplified using the WT-Ovation™ Applause WT/Amp RNA amplification system (NuGEN Technologies,) following the manufacturer’s instructions. Sense strand cDNA was fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.
Project description:Gene expression in wild-type and p38a-knockout keratinocytes were compared. Keratinocytes were isolated from newborn mice, and left unirradiated (0 h) and irradiated (4 h) with ultraviolet-B (UVB). C57BL/6 wild-type mice, and keratinocyte-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary keratinocytes.
Project description:Notch1 deficient hair matrix keratinocytes have lower mitotic rates, resulting in smaller follicles with fewer cells. In addition, the ratio of melanocytes to keratinocytes is greatly reduced. Microarray was performed to study downstream mechanism of Notch1-deficiency Keywords: genetic modification
Project description:Gene expression in wild-type and p38a-knockout keratinocytes were compared. Keratinocytes were isolated from newborn mice, and left unirradiated (0 h) and irradiated (4 h) with ultraviolet-B (UVB). C57BL/6 wild-type mice, and keratinocyte-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary keratinocytes. Gene expression in keratinocytes was analyzed 0 and 4 h after UVB irradiation (75 mJ/cm2).
Project description:Purpose: The goal of this study is to assess the transcriptomic changes induced by the loss BCL10/MALT1 signaling in keratinocytes and ist effect on IL-17A stimulation Methods: Keratinocytes were isolated from newborn Bcl10+/− and Bcl10−/− mice, cultured for 5 days, stimulated with IL-17A for 5 hours and harvested for RNA isolation. mRNA profiles were generated by deep sequencing, using Illumina NextSeq 550. Results: as shown by Gene Set Enrichment Analysis, IL-17A stimulation induced significant enrichment of an IL17 signature defined by Chiricozzi et al (JID 2011) in both Bcl10+/− and Bcl10−/− murine keratinocytes. However, direct comparison of Bcl10+/− and Bcl10−/− keratinocytes demonstrated a stronger enrichment of this signature in Bcl10 competent keratinocytes than in Bcl10 deficient cells.
Project description:As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/). We compared the gene expression profiles of uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ (KO), Prdm16LacZ/+(HET), and Prdm16+/+ (WT) mice.
Project description:Maternal stress has long been associated with lower birthweight but mechanisms remain elusive. This study explored how maternal stress may impact changes in gene expression within a cohort of mother-placenta-newborn triads in the eastern Democratic Republic of Congo We used microarrays to detail the global programme of gene expression underlying the impact of maternal stress on newborn birthweight and identified that global placental gene expression may partially mediate the negative impact of maternal war stress on newborn birthweight.