Endothelial Arid1a Deletion Disrupts the Balance among Angiogenesis, Neurogenesis, and Astrogenesis in the Developing Brain
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA913147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22768337_1.fastq.gz | Fastqsanger.gz | |||
| SRR22768337_2.fastq.gz | Fastqsanger.gz | |||
| SRR22768338_1.fastq.gz | Fastqsanger.gz | |||
| SRR22768338_2.fastq.gz | Fastqsanger.gz |
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Project description:Purpose:To gain futher insight into how endothelial Arid1a regulates the angiogenesis, neurogenesis, and astrogenesis,RNA-seq was used to analyze the genome-wide changes resulting from isolated endothelial cells of E15 Arid1a endothelial conditional knockout mice and littermate wild-type. Methods: mRNA from E15 isolated endothelial cells of Arid1afl/fl and Arid1acKO-Tie2 mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately one six thousand transcripts showed differential expression between the Arid1afl/fl and Arid1acKO-Tie2 mice brain cortex, with a fold change ≥2 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development process and regulation of cell communication.The down-regulated genes exhibited enrichment of biological processes related to cell movement. These results reflected endothelial Arid1a plays a vital role in cortex development. Conclusions: Endothelial Arid1a RNA-seq would provide a overall understanding how endothelial Arid1a regulates the Balance among angiogenesis, neurogenesis, and astrogenesis in the developing Brain
2022-12-21 | GSE221176 | GEO
Project description:The vascular system and the neural system processes occur simultaneously, the interaction among them is fundamental to the normal development of the central nervous system. Arid1a (AT-rich interaction domain 1A), which encodes an epigenetic subunit of the SWI/SNF chromatin-remodelling complex, is associated with promoter-mediated gene regulation and histone modification. However, the molecular mechanism of the interaction between cerebrovascular and neural progenitor cells (NPCs) remains unclear. To generate Arid1acKO-Tie2 mice, Arid1afl/fl mice were hybridized with Tie2-Cre mice. The Angiogenesis, neurogenesis and gliogenesis were studied by immunofluorescence staining and Western blotting. RNA-seq, RT-PCR, Western blotting, CO-IP and rescue experiments were performed to dissect the molecular mechanisms of Arid1a regulates fate determination of NPCs. We found that the absence of Arid1a results in increased the density of blood vessels, delayed neurogenesis and decreased gliogenesis, even after birth. Mechanistically, the deletion of Arid1a in endothelial cells causes a significant increase in H3k27ac and the secretion of maternal protein 2 (MATN2). In addition, matn2 alters the AKT/SMAD4 signalling pathway through its interaction with the NPCs receptor EGFR, leading to the decrease of SMAD4. SMAD complex further mediates the expression of downstream targets, thereby promoting neurogenesis and inhibiting gliogenesis. This study suggests that endothelial Arid1a tightly controls fate determination of NPCs by regulating the AKT-SMAD signalling pathway.
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Project description:Purpose:T To investigate the role of CCDC25 in the development of cortical nerves Methods: mRNA from E13 neural steneural stem cell were obtained. Culture in vitro for 4 days, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately one thousand transcripts showed differential expression between the control and knock down brain cortex, with a fold change ≥2 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development process and regulation of cell communication.The down-regulated genes exhibited enrichment of biological processes related to cell movement. These results reflected ccdc25 plays a vital role in cortex development. Conclusions: Endothelial Arid1a RNA-seq would provide a overall understanding how endothelial Arid1a regulates the Balance among angiogenesis, neurogenesis, and astrogenesis in the developing Brain
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Project description:A balance between angiogenesis inducers and inhibitors in the microenvironment controls the rate of new blood vessel formation. We hypothesized that fibroblasts, an important cellular constituent of the tissue stroma, secrete molecules that contribute to this balance. We further hypothesized that fibroblasts secrete molecules that promote angiogenesis when they are in a proliferative state and molecules that inhibit angiogenesis when they are not actively cycling (quiescent). Microarray analysis revealed that angiogenesis inducers and inhibitors are regulated as fibroblasts transition into a quiescent state and reenter the cell cycle in response to changes in serum. To assess whether changes in transcript levels result in changes in the levels of secreted proteins, we collected conditioned medium from proliferating and quiescent fibroblasts and performed immunoblotting for selected proteins. Secreted protein levels of the angiogenesis inhibitor pigment epithelium derived factor (PEDF) were higher in quiescent than proliferating fibroblasts. Conversely, proliferating fibroblasts secreted increased levels of the angiogenesis inducer vascular endothelial growth factor-C (VEGF-C). For the angiogenesis inhibitor thrombospondin-2, quiescent cells secreted a prominent 160 kDa form in addition to the 200 kDa form secreted by proliferating and restimulated fibroblasts. Using immunohistochemistry we discovered that fibroblasts surround blood vessels and that the angiogenesis inhibitor PEDF is expressed by quiescent fibroblasts in uterine tissue, supporting a role for PEDF in maintaining quiescence of the vasculature. This work takes a new approach to the study of angiogenesis by examining the expression of multiple angiogenesis regulators secreted from a key stromal cell, the fibroblast. mRNAs were analyzed by two color microarray from a human neonatal dermal fibroblasts cell line over a timecourse of serum starvation and serum restimulation.
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Project description:The study identifies genes that are regulated by the loss of the chromatin remodeller subunit ARID1A in colorectal cancer cell lines. This gene is frequently mutated in colorectal cancer.
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Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver and other adult tissues results in improved organ regeneration. Within SWI/SNF complexes, Arid1a physically interacts with C/ebpα, a hepatocyte transcription factor that drives maturation and limits proliferation. Genome-wide analysis showed that loss of Arid1a reduces the recruitment and activity of C/ebpα on target promoters, resulting in expression programs that favor regeneration and cellular fitness during injury. Arid1a binding is enriched in promoters near transcriptional start sites (TSSs), and C/ebpα binds at precisely the same positions, indicating that Arid1a facilitates C/ebpα binding across the genome. Perfuse and isolate primary hepatocytes from mice livers, analysis of genomic occupancy of C/ebpα and H3K4me2 in hepatocytes from Arid1a WT and Arid1a liver specific KO mice by ChIP-seq. Analysis of genomic occupancy of Arid1a in the hepatocytes from V5-Arid1a transgenic mouse by ChIP-seq.
2016-03-30 | E-GEOD-65167 | biostudies-arrayexpress
Project description:ARID1A, an epigentic modifier, is often mutated in ovarian clear cell carcinoma (OCCC). In addition, EZH2 is frequently upregulated in OCCC. Inhibtion of EZH2 with an inhibitor (GSK126) selectively inhibits ARID1A-mutated cells. This study was designed to understand changes in gene expression profiles following EZH2 inhibition or ARID1A restoration. Chromatin remodelers such as ARID1A are frequently mutated in a broad array of cancers. However, targeted cancer therapy based on ARID1A mutation status has not been described. Intriguingly, ARID1A mutated cancers typically lack genomic instability, suggesting significant involvement of epigenetic mechanisms. Here we show that inhibition of the EZH2 methyltransferase acts in a synthetic lethal manner in ARID1A mutated cells. Remarkably, ARID1A mutation status correlated with response to EZH2 inhibitor. Genome-wide profiling revealed antagonistic roles of ARID1A and EZH2 in gene regulation. Further, we identified PIK3IP1 as a direct ARID1A/EZH2 target gene whose upregulation contributes to the observed synthetic lethality in the EZH2 inhibitor treated ARID1A mutated cells. Significantly, EZH2 inhibitor caused the regression of established ARID1A mutated tumors in vivo. Together, this data demonstrate a synthetic lethality between ARID1A mutation and EZH2 inhibition. They indicate that pharmacological inhibition of EZH2 represents a novel treatment strategy for ARID1A mutated cancers.
2015-01-20 | E-GEOD-54979 | biostudies-arrayexpress
Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen) Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.
2012-05-31 | E-GEOD-38380 | biostudies-arrayexpress
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