Activation of a neural stem cell transcriptional program in parenchymal astrocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB39117 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4299220_1.fastq.gz | Fastqsanger.gz | |||
| ERR4299220_2.fastq.gz | Fastqsanger.gz | |||
| ERR4299230_1.fastq.gz | Fastqsanger.gz | |||
| ERR4299230_2.fastq.gz | Fastqsanger.gz | |||
| ERR4299240_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 952 |
Similar Datasets
Project description:Neural stem cells, located in discrete niches in the adult brain, generate new neurons throughout life. These stem cells are specialized astrocytes, but astrocytes in other brain regions (parenchymal astrocytes) do not generate neurons under physiological conditions. After stroke, however, astrocytes in the mouse striatum undergo neurogenesis, triggered by decreased Notch signaling. Notch signaling can be experimentally depleted in mice by deleting the Notch-mediating transcription factor Rbpj. This dataset consists of single-cell RNA sequencing data of astrocytes isolated from the striatum (where astrocytes undergo neurogenesis in response to Rbpj deletion) or somatosensory cortex (where astrocytes don't complete neurogenesis in response to Rbpj deletion) of 4 mice. Cells were isolated from Cx30-CreER; R26-tdTomato; Rbpj(fl/fl) mice at three time points after tamoxifen-induced Rbpj deletion (2, 4, 8 weeks), and from Cx30-CreER; R26-tdTomato mice with intact Rbpj 3 days after tamoxifen. These time points span the transition from astrocyte through transit-amplifying cells to neuroblasts. The dataset contains 1) astrocytes from the striatum that initiate a neurogenic transcriptional program in response to Rbpj deletion and generate transit-amplifying cells and neuroblasts, and 2) astrocytes from the somatosensory cortex that initiate a neurogenic program in response to Rbpj deletion but fail to generate transit-amplifying cells or neuroblasts.
2020-08-01 | E-MTAB-9268 | biostudies-arrayexpress
Project description:Adult neural stem cells, located in discrete brain regions, generate new neurons throughout life. These stem cells are specialized astrocytes, but astrocytes in other brain regions do not generate neurons under physiological conditions. After stroke, however, striatal astrocytes undergo neurogenesis in mice, triggered by decreased Notch signaling. We used single-cell RNA sequencing to characterize neurogenesis by Notch-depleted striatal astrocytes in vivo. Striatal astrocytes were located upstream of neural stem cells in the neuronal lineage. As astrocytes initiated neurogenesis, they became transcriptionally very similar to subventricular zone stem cells, progressing through a near-identical neurogenic program. Surprisingly, in the non-neurogenic cortex, Notch-depleted astrocytes also initiated neurogenesis. Yet, these cortical astrocytes, and many striatal ones, stalled before entering transit-amplifying divisions. Infusion of epidermal growth factor enabled stalled striatal astrocytes to resume neurogenesis. We conclude that parenchymal astrocytes are latent neural stem cells and that targeted interventions can guide them through their neuronal differentiation.
| S-EPMC7440914 | biostudies-literature
Project description:Ectopic expression of the reprogramming factors OCT4, SOX2, or NANOG into human astrocytes in specific cytokine/culture conditions activated the neural stem gene program and induced generation of cells expressing neural stem/precursor markers. Here we compare the whole gene expression profile of primary human astrocytes (Astro) with neural stem cells (HNSC) derived from astrocytes reprogramming
2013-12-01 | E-GEOD-36145 | biostudies-arrayexpress
Project description:Ectopic expression of the reprogramming factors OCT4, SOX2, or NANOG into human astrocytes in specific cytokine/culture conditions activated the neural stem gene program and induced generation of cells expressing neural stem/precursor markers (ASTRO-NSC). To evaluate the epigenetic changes associated with this reprogramming, we analyzed the DNA methylation patterns of Astro-NSC relative to untransfected astrocytes. We compared three human AstroNANOG-NSC clones to the astrocytes from which they were derived using NimbleGen 3x720K CpG Island Plus RefSeq Promoter Arrays
2013-01-05 | E-GEOD-42908 | 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:Ectopic expression of the reprogramming factors OCT4, SOX2, or NANOG into human astrocytes in specific cytokine/culture conditions activated the neural stem gene program and induced generation of cells expressing neural stem/precursor markers.
2013-12-01 | GSE36145 | GEO
Project description:Ectopic expression of the reprogramming factors OCT4, SOX2, or NANOG into human astrocytes in specific cytokine/culture conditions activated the neural stem gene program and induced generation of cells expressing neural stem/precursor markers (ASTRO-NSC). To evaluate the epigenetic changes associated with this reprogramming, we analyzed the DNA methylation patterns of Astro-NSC relative to untransfected astrocytes.
2013-01-05 | GSE42908 | GEO
Project description:Alveolar epithalial cells (A549) were used as a model of pulmonary parenchymal cell activation to quiery gene expression profile of activation with either cyclic stretch (20% elongation), TNF (20 ng/ml), LPS (1 mcg/ml) or TNF+STRETCH at both 1 and 4 hrs. Keywords: time-course
2004-10-03 | GSE1541 | GEO
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.
2015-09-16 | GSE73022 | GEO
Project description:Pancreatic cancer is characterized by a high frequency of cachexia, pain and neural invasion (N-inv). Neural damage is occurred by N-inv and modulates pain and muscle atrophy via the activation of astrocyte in the connected spine. The activated astrocyte by N-inv, thus, may affect cachexia in pancreatic cancer. Clinical studies in patients and autopsy cases with pancreatic cancer have revealed that N-inv is related to cachexia and astrocytic activation. We established a novel murine model of cancer cachexia using N-inv of human pancreatic cancer cells. Mice with N-inv showed a loss of body weight, skeletal muscle, and fat mass without appetite loss, which are compatible with an animal model of cancer cachexia. Activation of astrocytes in the spinal cord connected with N-inv was observed in our model. Experimental cachexia was suppressed by disrupting neural routes or inhibiting the activation of astrocytes. These data provide the first evidence that N-inv induces cachexia via astrocytic activation of neural route in pancreatic cancer. We produced neural invasion (N-inv) model using intraneural injection of Capan-1 cells to left sciatic nerve of male SCID mouse. For controls, subcutaneous model (SC) and PBS model were produced. Microarray analysis was performed using the first lumbar cord (L1) from PBS, SC, and N-inv mice at 6 w (n = 2 each).
2011-12-07 | E-GEOD-34189 | biostudies-arrayexpress