Project description:PPARgamma null (PpargΔ/Δ) mice present a generalized lipoatrophy and a dramatic skin phenotype, characterized by delayed hair morphogensis and the appearance, at adult age, of severe inflammatory infiltration. To investigate the molecular mechanisms underlying the delayed hair morphogenesis observed in PpargΔ/Δ mice, we used microarrays to detail the global program of gene expression in full thickness skin of PpargΔ/Δ mice and respective control mice at embryionic stage E17.5.
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
Project description:Transcriptional profile of full thickness skin or epidermis only obtained from K14-CreER+/+;GPX4flox mouse model vs K14-CreER-/-;GPX4flox controls is analyzed and compared to transcriptional profile of epidermis plus papillary dermis obtained from patient-matched lesional vs perilesional psoriatic skin.
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Hearts were taken from wide type and Myc-null Mouse embryos at E13.5 under the dissecting scope. Cardiac myocyte RNA was isolated using TRIZOL®Reagent Total RNA (100 ng) was hybridized to the Sentrix® MouseRef-8 Expression BeadChip that contains probes for ~24,000 transcripts. GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A. The data were analyzed with Illumina Inc. BeadStudio version 1.5.0.34 and normalized by rank invariant method.
Project description:We generated single cell transcriptomes from full thickness skin biopsies in mouse to quantify the skin cell types found in this species (control samples). To study how mouse skin changes upon exposure to a carcinogen, we performed a classical two-stage skin carcinogenesis experiment, wherein cancer is initiated by a single application of 7,12-dimethylbenz[a]-anthracene (DMBA) followed by repeated treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) to drive cell proliferation. After 10 weeks, full thickness skin biopsies were collected and used to generate single cell transcriptomes (treatment samples).
