Expression data from primary keratinocytes obtained from WT and keratinocyte specific Glut1-deficient mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE102955 | GEO | 2018/01/01
SECONDARY ACCESSION(S): PRJNA399529
REPOSITORIES: GEO
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Project description:Glut1 is highly expressed in basal cells of keratinocytes, but the regulation of Glut1 and expression of additional glucose transporters in the skin has not been explored, here we specifically ablate Glut1 in epidermal keratinocytes to elucidate the role of glucose transport in the keratinocytes. we performed microarray analysis in WT and Glut1 deficient primary keratinocytes to determine the pathways might contribute to the impaired proliferation in Glut1 deficient keratinocytes.
2018-01-01 | GSE94884 | GEO
Project description:Expression data from primary keratinocytes obtained from WT and keratinocyte specific Glut1-deficient mice
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Project description:Glut1 is highly expressed in basal cells of keratinocytes, but the functions and regulation of Glut1 has not been explored, here we specifically ablate Glut1 in epidermal keratinocytes to elucidate the role of glucose transport in the skin. We performed microarray analysis in WT and Glut1 deficient primary keratinocytes to determine the pathways might contribute to the impaired proliferation in Glut1 deficient keratinocytes,
2018-01-01 | GSE102953 | GEO
Project description:MED1 (Mediator complex subunit 1) is expressed by human epidermal keratinocytes and functions as a coactivator of several transcription factors. To elucidate the role of MED1 in keratinocytes, we established keratinocyte-specific MED1-null (MED1epi-/-) mice using the K5Cre-LoxP system. To elucidate the mechanism(s) underlying abnormalities of keratinocytes derived from MED1epi-/- mice, we compared the gene expression patterns of MED1epi-/--derived keratinocytes with their wild type counterparts by microarray analysis.
2012-09-02 | GSE35406 | GEO
Project description:MED1 (Mediator complex subunit 1) is expressed by human epidermal keratinocytes and functions as a coactivator of several transcription factors. To elucidate the role of MED1 in keratinocytes, we established keratinocyte-specific MED1-null (MED1epi-/-) mice using the K5Cre-LoxP system. To elucidate the mechanism(s) underlying abnormalities of keratinocytes derived from MED1epi-/- mice, we compared the gene expression patterns of MED1epi-/--derived keratinocytes with their wild type counterparts by microarray analysis. Generation of the MED1 conditional null mutation in epidermal keratinocytes and cell culture: MED1flox/flox mice (Jia et al, J Biol Chem 279:24427. 2004) were mated with K5Cre mice (Tarutani et al, Proc Natl Acad Sci U S A 94:7400. 1997) to generate F1 K5Cre+;MED1flox/+ mice. The K5Cre+;MED1flox/+ mice were then mated with MED1flox/flox mice to generate K5Cre+;MED1flox/flox mice (MED1epi-/-). Mice were screened for presence of the transgene by PCR using specific primers for the floxed MED1 gene and the human K5 gene according to the previous reports. Skin of newborn mice was excised after the mice were sacrificed with excessive anesthetic and were treated with dispase followed by trypsin to separate the epidermis from the dermis. Keratinocytes were seeded on type I collagen coated dishes, and were cultured in CnT07 conditioned culture medium (CELLnTEC, Bern, Switzerland). Keratinocytes were used for the experiment as a primary culture. All animal studies were conducted according to protocols approved by the Institutional Animal Care and Use Committee at Osaka University. Microarray analysis: For comprehensive comparison of gene expression patterns between keratinocytes derived from MED1epi-/- and from WT mice, microarray analysis was used. Total RNAs were extracted using an RNeasy kit (Qiagen, San Diego, CA). Then, 2μg total RNA was reverse transcribed to cDNA with T7 oligo d(T) primer (Affymetrix, Santa Clara, CA). The cDNA synthesis products were used for in vitro transcription reactions containing T7 RNA polymerase and biotinylated nucleotide analogue (pheudouridine base) cRNAs. The labeled cRNA products were then fragmented and loaded onto GeneChip(R) Mouse Genome 430 2.0 arrays (Affymetrix), and were hybridized according to the manufacturer’s protocol. Streptavidin-Phycoerythrin (Molecular Probes) was used as the fluorescent conjugate to detect hybridized target sequences. Raw intensity data from the GeneChip array were analyzed by GeneChip Operating Software (Affymetrix).
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Project description:Paucity of the glucose transporter-1 (Glut1) protein resulting from haploinsufficiency of the SLC2A1 gene arrests cerebral angiogenesis and disrupts brain function to cause Glut1 deficiency syndrome (Glut1 DS). Restoring Glut1 to Glut1 DS model mice prevents disease, but the precise cellular sites of action of the transporter, its temporal requirements, and the mechanisms linking scarcity of the protein to brain cell dysfunction remain poorly understood. Here, we show that Glut1 functions in a cell-autonomous manner in the cerebral microvasculature to affect endothelial tip cells and, thus, brain angiogenesis. Moreover, brain endothelial cell-specific Glut1 depletion not only triggers a severe neuroinflammatory response in the Glut1 DS brain, but also reduces levels of brain-derived neurotrophic factor (BDNF) and causes overt disease. Reduced BDNF correlated with fewer neurons in the Glut1 DS brain. Controlled depletion of the protein demonstrated that brain pathology and disease severity was greatest when Glut1 scarcity was induced neonatally, during brain angiogenesis. Reducing Glut1 at later stages had mild or little effect. Our results suggest that targeting brain endothelial cells during early development is important to ensure proper brain angiogenesis, prevent neuroinflammation, maintain BDNF levels, and preserve neuron numbers. This requirement will be essential for any disease-modifying therapeutic strategy for Glut1 DS.
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Project description:We conducted RNA sequencing analysis on skin tissues obtained from spontaneous inflammatory skin lesions in keratinocyte-specific Mettl3 knockout (K14CreERT2;Mettl3fl/fl) mice and their controls (Mettl3fl/fl). In brief, we observed spontaneous skin inflammation in the tail of K14CreERT2;Mettl3fl/fl mice 2-3 weeks following tamoxifen injection. The objective of this study was to investigate the impact and underlying mechanism of Mettl3 in epidermal keratinocytes regarding skin inflammation
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Project description:PLA2G4D is a phospholipase and transacylase expressed in epidermal keratinocytes, and its expression is upregulated in inflammatory skin disorders such as psoriasis. Treatment of primary keratinocytes with proinflammarory cytokines IL17A and TNFα markedly increases Pla2g4d-mRNA expression. To investigate the function of PLA2G4D, we conducted bulk RNA sequencing of primary keratinocytes isolated from wild-type and Pla2g4d-deficient mice and studied transcriptional changes under basal and cytokine stimulation. The sequencing data suggests that PLA2G4D modulates fundamental biological processes including cell proliferation, differentiation, and signaling.
2024-10-17 | GSE277039 | GEO
Project description:Regulation of human keratinocyte (HK) migration is critical for skin wound healing. Profiling HK migration-specific genes could help us gain a comprehensive understanding of the process. The main challenge is to separate genes that are unrelated to migration, but simultaneously induced by the same growth factor. In this study, we took advantage of a unique response of HKs to transforming growth factor-beta (TGF-beta), which inhibits proliferation but not migration of HKs, to suppress selectively the proliferation-related genes. Furthermore we stimulated HKs independently with TGF-alpha or insulin and identified the common genes and eliminated TGF-alpha- or insulin-specific genes. Under these conditions, we obtained profiles of the immediate-early genes (IEGs, at 30 minutes), early genes (EGs, at 60 minutes), and delayed-early genes (DEGs, at 120 minutes) by microarray analyses, followed by quantitative real-time reverse transcription-PCR (QRT-PCR) validation and functional characterization by RNA interference (RNAi). Our results revealed the following: (1) 25 upregulated and 1 downregulated IEGs; (2) 58 upregulated and 15 downregulated EGs, and (3) 13 upregulated and 3 downregulated DEGs in both TGF-alpha- and insulin-stimulated HKs. Three genes, all encoding secreted molecules, were investigated in HK migration. These cell motility-specific gene profiles may prove useful to skin wound healing.
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