Gene Expression Analysis of Nestin-creERT2, or NG2-creERTM driven P53f/f; Nf1f/+; Ptenf/+ mouse GBM
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE127273 | GEO | 2020/03/31
REPOSITORIES: GEO
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Project description:Mouse model with P53f/f;Nf1f/+;Ptenf/+ configuration driven by Nestin-creERT2 and NG2-creERTM induced at 1 month postnatal forms high grade glioma in the brain. Tumors were harvested and total RNA were extracted for gene expression profile. Three tumors were harvested from the Nestin-creERT2 mouse model and 5 tumors were harvested from the NG2-creERTM mouse model with desired genotype when mice show neurological symptomes. Three control brain tissue for each model were harvested at corresponding anatomical position in the control mice. Total RNA were extracted from the tumor tissue and control tissue
2015-07-30 | E-GEOD-57038 | biostudies-arrayexpress
Project description:Mouse model with P53f/f;Nf1f/+;Ptenf/+ configuration driven by Nestin-creERT2 and NG2-creERTM induced at 1 month postnatal forms high grade glioma in the brain. Tumors were harvested and total RNA were extracted for gene expression profile.
2015-07-30 | GSE57038 | GEO
Project description:Gene Expression Analysis of Nestin-creERT2, or NG2-creERTM driven P53f/f Nf1f/+ Ptenf/+ mouse GBM
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Project description:RNA Sequencing Analysis of Nestin-creERT2, NG2-creERTM, and Synapsin-cre Tumors
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Project description:RNA sequencing analysis was performed on glioma primary tissue harvested from different mouse models
2018-12-04 | GSE117258 | GEO
Project description:NG2/CSPG4 is expressed in soft tissue sarcomas, however, its function in this tumor type, and its capacity to serve as a therapeutic target are unknown. Here, we used genetically engineered mice and cells from human tumors to determine the function of Ng2/Cspg4 in soft tissue sarcoma initiation and growth. We also investigated the potential for NG2/CSPG4 mAb immunotherapy to target human sarcomas established as xenografts in mice. Inhibiting Ng2/Cspg4 expression in established soft tissue sarcomas is associated with a smaller tumor volume and a reduction in cell proliferation. Intriguingly, deleting Ng2/Cspg4 at the time of tumor initiation has the opposite effect. Gene profiling found that Igfbp3/5 are substantially downregulated when Ng2/Cspg4 is depleted at the time of tumor initiation, but upregulated or only minimally downregulated when Ng2/Cspg4 is depleted after tumor initiation. Furthermore, the normal regulation of Igfbp is blunted when Ng2/Cspg4 is deleted at the time of tumor initiation. Our data show a difference in NG2/CSPG4 function in tumor initiation and maintenance, and provides pre-clinical evidence supporting NG2/CSPG4 as a therapeutic approach in soft tissue sarcoma.
2017-04-07 | GSE97489 | GEO
Project description:Changes in the mechanical homeostasis of the temporomandibular joint (TMJ) can lead to the initiation and progression of degenerative arthropathies such as osteoarthritis (OA). Cells sense and engage with their mechanical microenvironment through interactions with the extracellular matrix. In the mandibular condylar cartilage, the pericellular microenvironment is composed of type VI collagen. NG2/CSPG4 is a transmembrane proteoglycan that binds with type VI collagen, and has been implicated in the cell stress response through mechanical loading-sensitive signaling networks including ERK 1/2. The objective of this study is to define the role of NG2/CSPG4 in the initiation and progression of TMJ OA and to determine if NG2/CSPG4 engages ERK 1/2 in a mechanical loading dependent manner. In vivo, we induced TMJ OA in control and NG2/CSPG4 knockout mice using a surgical destabilization approach. In control mice, NG2/CSPG4 is depleted during the early stages of TMJ OA and NG2/CSPG4 knockout mice have more severe cartilage degeneration, elevated expression of key OA proteases, and suppression of OA matrix synthesis genes. In vitro, we characterized the transcriptome and protein from control and NG2/CSPG4 knockout cells and found significant dysregulation of the ERK 1/2 signaling axis. To characterize the mechanobiological response of NG2/CSPG4, we applied mechanical loads on cell-agarose-collagen scaffolds using a compression bioreactor and illustrate that NG2/CSPG4 knockout cells fail to mechanically activate ERK 1/2 and are associated with changes in the expression of the same key OA biomarkers measured in vivo. Together, these findings implicate NG2/CSPG4 in the mechanical homeostasis of TMJ cartilage and in the progression of degenerative arthropathies including OA.
2022-09-24 | GSE214077 | GEO
Project description:Transcriptional profiling of subventricular zone (SVZ) progenitors comparing control healthy mice to mice induced to develop an autoimmune demyelination (EAE model). Goal was to unveil genes involved in demyelination-induced reactivity of SVZ progenitors. Two-condition experiment, healthy vs. EAE derived SVZ progenitors. Biological replicates: 2 control replicates, 2 EAE replicates. SVZ progenitors were sorted in two cell populations: neuronal progenitors (PSA-NCAM magnetic sorting) and glial progenitors (NG2 magnetic sorting). Progenitors from healthy mice are reference samples.
2013-09-09 | E-GEOD-47486 | biostudies-arrayexpress
Project description:Changes in the mechanical homeostasis of the temporomandibular joint (TMJ) can lead to the initiation and progression of degenerative arthropathies such as osteoarthritis (OA). Cells sense and engage with their mechanical microenvironment through interactions with the extracellular matrix. In the mandibular condylar cartilage, the pericellular microenvironment is composed of type VI collagen. NG2/CSPG4 is a transmembrane proteoglycan that binds with type VI collagen, and has been implicated in the cell stress response. The objective of this study is to define the role of NG2/CSPG4 in the cell stress response during serum starvation. To evaluate the role of the NG2/CSPG4, primary mandibular fibrochondrocytes from c57 BL/6 J and NG2/CSPG4 knockout mice (mixed sex) were cultured in normal and serum starvation conditions. To evaluate the role of the NG2/CSPG4 ectodomain, primary mandibular fibrochondrocytes were immortalized using hTERT. CRSIPR/Cas9 was used to truncate the NG2/CSPG4 ectodomain by targeting the type VI collagen binding region. Normal culture conditions were AMEM growth media supplemented with 10% FBS, penicillin, L-Glut, and plasmocin. Serum starvation conditions were Optimem media with no FBS, supplemented with penicillin, L-Glut, and plasmocin. Serum starvation was induced for 24 hours. RNA from the cells was isolated using the RNeasy kit (Qiagen). poly(A) RNA was fragmented using divalent cation buffer in elevated temperature. The DNA library construction is shown in the following workflow. Quality control analysis and quantification of the sequencing library were performed using Agilent Technologies 2100 Bioanalyzer High Sensitivity DNA Chip. Paired-ended sequencing was performed on Illumina’s NovaSeq 6000 sequencing system. Sequencing was done by LC Sciences. These data illustrate that in serum starvation conditions, NG2/CSPG4 knockout mandibular fibrochondrocytes and targeted truncation of the NG2/CSPG4 ectodomain alters the transcriptional profile of the cell, promoting biological processes associated with cell stress, migration, and ossiciation.
2023-11-30 | GSE245589 | GEO
Project description:Changes in the mechanical homeostasis of the temporomandibular joint (TMJ) can lead to the initiation and progression of degenerative arthropathies such as osteoarthritis (OA). Cells sense and engage with their mechanical microenvironment through interactions with the extracellular matrix. In the mandibular condylar cartilage, the pericellular microenvironment is composed of type VI collagen. NG2/CSPG4 is a transmembrane proteoglycan that binds with type VI collagen, and has been implicated in the cell stress response. The objective of this study is to define the role of NG2/CSPG4 in the cell stress response during serum starvation. To evaluate the role of the NG2/CSPG4, primary mandibular fibrochondrocytes from c57 BL/6 J and NG2/CSPG4 knockout mice (mixed sex) were cultured in normal and serum starvation conditions. To evaluate the role of the NG2/CSPG4 ectodomain, primary mandibular fibrochondrocytes were immortalized using hTERT. CRSIPR/Cas9 was used to truncate the NG2/CSPG4 ectodomain by targeting the type VI collagen binding region. Normal culture conditions were AMEM growth media supplemented with 10% FBS, penicillin, L-Glut, and plasmocin. Serum starvation conditions were Optimem media with no FBS, supplemented with penicillin, L-Glut, and plasmocin. Serum starvation was induced for 24 hours. RNA from the cells was isolated using the RNeasy kit (Qiagen). poly(A) RNA was fragmented using divalent cation buffer in elevated temperature. The DNA library construction is shown in the following workflow. Quality control analysis and quantification of the sequencing library were performed using Agilent Technologies 2100 Bioanalyzer High Sensitivity DNA Chip. Paired-ended sequencing was performed on Illumina’s NovaSeq 6000 sequencing system. Sequencing was done by LC Sciences. These data illustrate that in serum starvation conditions, NG2/CSPG4 knockout mandibular fibrochondrocytes and targeted truncation of the NG2/CSPG4 ectodomain alters the transcriptional profile of the cell, promoting biological processes associated with cell stress, migration, and ossiciation.
2024-10-30 | GSE245590 | GEO