Common myeloid progenitor cells from murine bone marrow were sorted according to ROS content using FACS with H2-DCFDA staining.
Intracellular reactive oxygen species mark and influence the megakaryocyte-erythrocyte progenitor fate of common myeloid progenitors.
Specimen part
View SamplesWe examined the adherence-mediated signaling of meningococci to human cells by comparing gene expression profiles of primary human umbilical vein endothelial cells (HUVEC) infected by piliated and adherent wild-type (WT), frpC/frpA-deficient mutant, or the non-adherent (pilD) N. meningitidis MC58 bacteria defective in production of the type IV pilus, respectively. Surprisingly, no significant difference was found between the transcriptomes of HUVECs infected by bacteria producing, or not the RTX FrpC and FrpA proteins, thus failing to provide any hints on their biological activity. In contrast, pili-mediated adhesion of meningococci resulted in alterations of expression levels of human genes known to regulate apoptosis, cell proliferation, inflammatory response or adhesion. In particular, genes for signaling pathway proteins involved in early embryonic development, such as transforming growth factor- (TGF-)/Smad, Wnt/-catenin, and Notch/Jagged were found to be upregulated upon adhesion of N. meningitidis together with genes for a number of transcription factors. This reveals that adhering piliated meningocci manipulate signaling pathways controlling human cell proliferation, survival and defense mechanisms, while establishing a commensal relationship with the host.
Meningococcal adhesion suppresses proapoptotic gene expression and promotes expression of genes supporting early embryonic and cytoprotective signaling of human endothelial cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Effect of orally administered collagen hydrolysate on gene expression profiles in mouse skin: a DNA microarray analysis.
Sex, Age, Specimen part, Treatment
View SamplesDietary collagen hydrolysate has been conjectured to improve skin barrier function. To investigate the effect of long-term collagen hydrolysate administration on the skin, we evaluated stratum corneum water content and skin elasticity in intrinsic aged mice. Female 9-week-old hairless mice were fed a control diet, or a collagen hydrolysate-containing diet, for 12 weeks. The stratum corneum water content and skin elasticity were sequentially decreased by chronological aging in control mice. Intake of collagen hydrolysate significantly suppressed such changes. Moreover, we comprehensively analyzed gene expression in the skin of mouse, which had been administered collagen hydrolysate, using DNA microarray. Twelve weeks after start of collagen intake, no significant differences appeared in gene expression profile compared to that of control group. However, 12 weeks after administration, 135 genes were up-regulated and 448 genes were down-regulated in collagen group compared to control group. It is indicate that gene changes preceded changes of barrier function and elasticity. We focused on several genes correlated with functional changes in the skin. Gene Ontology terms, especially related to epidermal cell development, were signicantly enriched in up-regulated genes. These skin function-related genes had properties that facilitate epidermal production and differentiation and suppress dermal degradation. Thus, dietary collagen hydrolysate induced positive gene changes. In conclusion, our results suggest that alteration of gene expression at early stages after collagen administration affect skin barrier function and mechanical properties. Long-term oral intake of collagen hydrolysate improves skin dysfunction by regulating genes related to production and maintenance of the skin tissue.
Effect of orally administered collagen hydrolysate on gene expression profiles in mouse skin: a DNA microarray analysis.
Sex, Age, Specimen part, Treatment
View SamplesDietary collagen hydrolysate has been conjectured to improve skin barrier function. To investigate the effect of long-term collagen hydrolysate administration on the skin, we evaluated stratum corneum water content and skin elasticity in intrinsic aged mice. Female 9-week-old hairless mice were fed a control diet, or a collagen hydrolysate-containing diet, for 12 weeks. The stratum corneum water content and skin elasticity were sequentially decreased by chronological aging in control mice. Intake of collagen hydrolysate significantly suppressed such changes. Moreover, we comprehensively analyzed gene expression in the skin of mouse, which had been administered collagen hydrolysate, using DNA microarray. Twelve weeks after start of collagen intake, no significant differences appeared in gene expression profile compared to that of control group. However, 1 week after administration, 135 genes were up-regulated and 448 genes were down-regulated in collagen group compared to control group. It is indicate that gene changes preceded changes of barrier function and elasticity. We focused on several genes correlated with functional changes in the skin. Gene Ontology terms, especially related to epidermal cell development, were signicantly enriched in up-regulated genes. These skin function-related genes had properties that facilitate epidermal production and differentiation and suppress dermal degradation. Thus, dietary collagen hydrolysate induced positive gene changes. In conclusion, our results suggest that alteration of gene expression at early stages after collagen administration affect skin barrier function and mechanical properties. Long-term oral intake of collagen hydrolysate improves skin dysfunction by regulating genes related to production and maintenance of the skin tissue.
Effect of orally administered collagen hydrolysate on gene expression profiles in mouse skin: a DNA microarray analysis.
Sex, Age, Specimen part, Treatment
View SamplesBmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells.
Poised lineage specification in multipotential hematopoietic stem and progenitor cells by the polycomb protein Bmi1.
Specimen part
View SamplesTo analyze target genes of human heat shock transcription factor 1 (HSF1), we first generated two independent HeLa clones (RDT1 and RDT2) expressing an actively mutated hHSF1 (hHSF1RDT), which lacks the regulatory domain that masks its activation domain and possesses a glutamic acid at amino acid 395 instead of a leucine in the suppression domain of the trimerization domain (Fujimoto et al., J. Biol. Chem. 280, 34908-34916, 2005). We also generated a HeLa clone expressing chicken HSF1 (HeLa/cHSF1) to compare its profile of gene expression with those of RDT1 and RDT2 cells (Nakai and Morimoto, Mol. Cell. Biol. 13, 1983-1997, 1993). We then carried out DNA microarray analysis using total RNA isolated from HeLa, HeLa/cHSF1, RDT1, and RDT2 cells grown under normal growth conditions.
Heat shock factor 1 ameliorates proteotoxicity in cooperation with the transcription factor NFAT.
Cell line
View SamplesFus is the gene for a member of the FET family of RNA-binding proteins often involved in chromosomal translocations to generate oncogenic fusion genes in human cancers. Fus participates in multiple cellular functions, including RNA processing and transport, transcriptional regulation, and genome integrity. We uncovered its critical role in the maintenance of hematopoietic stem cells (HSCs). Fus-/- fetal livers developed normally except for a mild reduction in numbers of colony-forming cells compared to the wild type. The proliferation and differentiation of Fus-/- hematopoietic progenitors were normal in vitro. However, the number of colony-forming cells present in long-term cocultures of Fus-/- hematopoietic progenitors and stromal cells was significantly reduced. Fus-/- HSCs had an impaired long-term repopulating capacity and failed to repopulate in tertiary recipient mice. Fus-/- HSCs were highly susceptible to radiation both in vitro and in vivo and showed retardation of radiation-induced DNA damage repair. These findings define Fus as a novel regulator of HSCs and implicate it in stress-resistance and maintenance of the genomic integrity of HSCs. Therefore, it would be of importance to analyze the gene expression profiles of Fus-knockout hematopoietic stem/progenitor cells to understand its role in HSCs.
FET family proto-oncogene Fus contributes to self-renewal of hematopoietic stem cells.
Specimen part
View SamplesCD4+T cells are differentiated into Th1, Th2, Th17 and Treg cells after Antigen presentation by other cell types such as dendritic cells, macrophages and B cells in Lymph nodes. Those differentiated CD4+T cells are subdivided into cell subsets by their producing cytokines and surface markers. We recently identified that ST2 expressing Th2 cells highly produced IL-5 comparing to ST2- Th2 cells in helminth infection. In this study, we investigated the RNAseq analysis to characterize these Th2 cells. Overall design: Characterization of ST2+ and ST2- mTh cells are assessed by RNA-seq.
CXCR6<sup>+</sup>ST2<sup>+</sup> memory T helper 2 cells induced the expression of major basic protein in eosinophils to reduce the fecundity of helminth.
Specimen part, Cell line, Subject
View SamplesBmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells.
Lethal myelofibrosis induced by Bmi1-deficient hematopoietic cells unveils a tumor suppressor function of the polycomb group genes.
Specimen part
View Samples