Expression of rat hepatocytic progenitor cells with and without hepatic Thy1-positive cells in retrorsine/partial hepatectomy treated rats models.
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Norihisa Ichinohe
PROVIDER: E-GEOD-85577 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We used microarrays to characterize the global changes in gene expression in C2C12 cells due to siRNA knockdown of long non-coding RNA H19 Control siRNA or siRNA specific for mouse H19 were transfected into day1 differentiating C2C12 myoblasts in triplicates. 40 H later total RNAs were isolated and subjected with microarray analysis.
2013-09-30 | E-GEOD-49535 | biostudies-arrayexpress
Project description:Brain inflammation, a common feature in neurodegenerative diseases, is a complex series of events, which can be detrimental and even lead to neuronal death. Nonetheless, several studies suggest that inflammatory signals are also positively influencing neural cell proliferation, survival, migration and differentiation. Recently, correlative studies suggested that astrocytes are able to dedifferentiate upon injury, and may thereby re-acquire neural stem cells (NSC) potential. However, the mechanism underlying this dedifferentiation process upon injury remains unclear. In this study, we find that during the early response of reactive gliosis, inflammation induces a conversion of mature astrocytes into neural progenitors. A TNF treatment induces the decrease of specific astrocyte markers, such as GFAP or genes related to glycogen metabolism, while a subset of these cells re-express immaturity markers, such as CD44, Musashi-1 and Oct4. Thus, TNF treatment results in the appearance of cells that exhibit a neural progenitor phenotype and are able to proliferate and differentiate into neurons and/or astrocytes. This dedifferentiation process is maintained as long as TNF is present in the culture medium. In addition, we identify a role for Oct4 in this process, since the TNF-induced dedifferentiation can be prevented by inhibiting Oct4 expression. Our results show that activation of the NF-kB pathway through TNF plays an important role in the dedifferentiation of astrocytes via the re-expression of Oct4. These findings indicate that the first step of reactive gliosis is in fact a dedifferentiation process of resident astrocytes mediated by the NF-kB pathway. This dedifferentiation process is maintained as long as TNF is present in the culture medium. In addition, we identify a role for Oct4 in this process, since the TNF-induced dedifferentiation can be prevented by inhibiting Oct4 expression. Our results show that activation of the NF-kB pathway through TNF plays an important role in the dedifferentiation of astrocytes via the re-expression of Oct4. These findings indicate that the first step of reactive gliosis is in fact a dedifferentiation process of resident astrocytes mediated by the NF-kB pathway. Cultures of primary mouse astrocytes were treated with TNF (50 ng/mL) for 24 hours. Cells were collected and immediately homogenized in cooled down RNA NOW reagent (OZYME). Total RNA was extracted according to RNA NOW manufacturer's recommendations with -20°C overnight incubation for small RNA precipitation. Total RNA integrity and purity were assessed using the Agilent 2100 Bioanalyzer and RNA 6000 Nano LabChip kits (Agilent Technologies). Only good-quality RNA (no contamination or degradation, RIN > 9) was used and further processed. Total RNA samples were reverse-transcribed to double-stranded cDNA using specific primers, which reduce the priming of rRNA. cRNA was generated by in vitro transcription and reverse transcribed into a sense single-stranded cDNA. The cDNA was fragmented, labeled, and hybridized onto Affymetrix GeneChip Mouse Gene 1.0 ST Arrays according to the Ambion Whole Transcript Expression kit for Affymetrix GeneChip Whole Transcript Expression Array Protocol (P/N 4425209 Rev.B 05/2009) and GeneChip WT Terminal Labeling and Hybridization User Manual for use with the Ambion Whole Transcript Expression kit (P/N 702808 Rev.6). Microarrays were then washed, stained, and scanned according to the manufacturer's instructions. The samples cover combinations of 7 time points (0H, 6H, 24H, 48H, 72H, 1W, 2W) and two conditions (TNF and control), with multiple replicates per condition and time point.
2015-09-16 | E-GEOD-73022 | biostudies-arrayexpress
Project description:We used microarrays to characterize the global changes in gene expression within the ascending aorta of mice due to conditional disruption of TGF-M-NM-2 signaling in smooth muscle and/or due to heterozygous fibrillin-1 mutation. Myh11-CreERT2.Tgfbr2f/f (abbreviated as Cre.Tgfbr2) mice were cross-bred to Fbn1C1039G/+ (abbreviated as Fbn1C/+) mice and treated with vehicle or tamoxifen for 5 d starting at 4 wk of age to generate 4 groups of animals: 1) Cre.Tgfbr2-Veh: controls with intact TGF-M-NM-2 signaling and wild-type fibrillin-1 expression; 2) Cre.Tgfbr2-Tmx: conditional disruption of Tgfbr2 in smooth muscle with wild-type fibrillin-1 expression; 3) Fbn1C1039G.Cre.Tgfbr2-Veh: heterozygous expression of mutant fibrillin-1 with intact TGF-M-NM-2 signaling; and 4) Fbn1C1039G.Cre.Tgfbr2-Tmx: conditional disruption of Tgfbr2 in smooth muscle with heterozygous expression of mutant fibrillin-1. The animals were euthanized at 6 weeks of age and their ascending aortas (from above the coronary arteries to the first arch branch) were collected and total RNA was extracted.
2013-05-31 | E-GEOD-36778 | biostudies-arrayexpress
Project description:Gene expression profile in CS1AN deficient and CSBwt restored cell lines after 24 hours of UV or alphe-amanitin treatment (only for restored). The comaprison of expression profile between 0 and 24 hours revealed continouse suppresion of transcription upon UV treatment in CS1AN cell line and alpha-amanitin treated CS1AN CSBwt restored cells. Gene expression profiles were obtained in duplicates for un-treated (assigned as 0h time point) and treated (assigned as 24h time point) cells.
2014-05-23 | E-GEOD-57923 | biostudies-arrayexpress
Project description:TIMP-4 overexpression increases tumor burden in mice, promotes progenitor cell phenotype and sensitizes cells to apoptosis, by relying on NFkB signaling We used microarrays to detail the molecules and signal transduction pathways modulated by hrTIMP-4
2015-11-25 | E-GEOD-60671 | biostudies-arrayexpress
Project description:To describe normal cardiac and brain development during late first and early second trimester in human fetuses using microarray and pathways analysis and the creation of a corresponding M-bM-^@M-^\normalM-bM-^@M-^] database. RNA from recovered tissues was used for transcriptome analysis with Affymetrix 1.0 ST microarray chip. From the amassed data we investigated differences in cardiac and brain development within the 10-18 GA period dividing the sample by GA in three groups: 10-12 (H1), 13-15(H2) and 16-18(H3) weeks. A fold change of 2 or above adjusted for a false discovery rate of 5% was used as initial cut-off to determine differential gene expression for individual genes. Test for enrichment to identify functional groups were carried out using the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Array analysis correctly identified the cardiac specific genes, and transcripts reported to be differentially expressed were confirmed by qRT-PCR. 14 hearts-10 brains
2014-05-21 | E-GEOD-56048 | biostudies-arrayexpress
Project description:Dorsal root ganglia (DRG, L3-L5) from either control mice or mice subjected to the CAIA model and treated twice weekly from day 12 with drug X or control solution were collected during the post-inflammatory phase of the model. RNA was extracted using a Qiagen RNeasy Mini Kit, subjected to GeneChip® ST Arrays (GeneChip® Mouse Gene 2.0 ST Array) analysis and assessed for presence of certain mRNA and/or group differences in mRNA levels.
2019-04-21 | E-MTAB-7853 | biostudies-arrayexpress
Project description:Multipotent stem cells and their lineage-restricted progeny drive nephron formation within the developing kidney. Validated markers of these early stem/progenitor populations are essential for deciphering their in vivo function and for evaluating their clinical potential for treating adult kidney disease. Here, we document expression of the adult stem cell marker Lgr5 in the developing kidney and assess the stem/progenitor identity of Lgr5+ve cells via in vivo lineage tracing. The appearance and localization of Lgr5+ve cells coincided with that of the S-shaped body around E14. Lgr5 expression remained restricted to cell clusters within developing nephrons in the cortex until P7, when expression was permanently silenced. In vivo lineage tracing identified Lgr5 as a marker of a novel progenitor population within nascent nephrons dedicated to generating the thick ascending limb of Henle's loop and distal convoluted tubule. The Lgr5 surface marker and experimental models described here will be invaluable for deciphering the contribution of early nephron stem cells to developmental defects and for isolating human nephron progenitors as a prerequisite to evaluating their therapeutic potential. Metanephric kidneys of timed pregnancies of ~14 days of gestation were harvested and cultured for ~10 days. Lgr5-EGFP-Ires-CreERT2-positive embryonic kidneys were identified by fluorescence microscopy and enzymatically digested to a single cell solution. GFPhi and GFPneg cells were sorted by flow cytometry (MoFlo; Dako). RNA, isolated using RNeasy (Qiagen), was analyzed using the Affymetrix platform.
2012-09-04 | E-GEOD-39881 | biostudies-arrayexpress
Project description:Half a brain hemisphere from adult male mice with Slc18b1 knocked out globally, was compared to brain from control littermates.
2019-11-10 | E-MTAB-8443 | biostudies-arrayexpress
Project description:Using microarray analysis, we explored the differences in gene expression profiles between individual and combined stimulation of Toll-like receptor 4 (TLR4) and Nucleotide oligomerization domain (NOD)-like receptor (NOD2) in THP-1 cells. Analysis was performed 3 hours post addition of TLR4 agonist MPLA and the NOD2 agonist MDP to THP-1 cells. The results provide the detailed molecular profile of the the genetic response to individual and combined stimulation of TLR4 and NOD2 receptors THP-1 cells (Invivogen) were seeded in 3-cm culture dishes at 1x10^6 cells per dish in RPMI medium. Next day, cells were treated with MDP (20μg/ml) and MPLA (1μg/ml) individually or in combination or left untreated.
2016-04-05 | E-GEOD-79900 | biostudies-arrayexpress