NG2/CSPG4 regulates the transcriptional profile of mandibular fibrochondrocytes during serum starvation [RNAseq-immortalized cells]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1029039 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR26411882_1.fastq.gz | Fastqsanger.gz | |||
| SRR26411882_2.fastq.gz | Fastqsanger.gz | |||
| SRR26411883_1.fastq.gz | Fastqsanger.gz | |||
| SRR26411883_2.fastq.gz | Fastqsanger.gz |
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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
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:NG2/CSPG4 regulates the transcriptional profile of mandibular fibrochondrocytes during serum starvation
| PRJNA1029036 | ENA
Project description:NG2/CSPG4 regulates the transcriptional profile of mandibular fibrochondrocytes during serum starvation [RNAseq-primary cells]
| PRJNA1029038 | ENA
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: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:The migration of mandibular fibrochondrocytes is important for the development of the mandible, the homeostasis of the mandibular cartilage, and for the capacity of the tissue to respond to injury. Mandibular fibrochondrocytes have to overcome formidable obstacles during migration including a dense and heterogeneous three-dimensional matrix. Guiding the direction of cell migration and commitment to a migratory phenotype in this microenvironment necessitates a multivalent response to chemotactic and extracellular matrix-mediated stimuli. One of the key matrix components in the cartilage of the temporomandibular joint is type VI collagen. Neuron/glial antigen 2 (NG2/CSPG4) is a transmembrane proteoglycan that binds with collagen VI and has been implicated in a wide range of cell behaviors including cell migration, motility, adhesion, and proliferation. While NG2/CSPG4 has been shown to be a key regulator of mandibular cartilage homeostasis, its role in the migration of mandibular fibrochondrocytes during normal and cell stress conditions has yet to be resolved. Here, we address this gap in knowledge by characterizing NG2/CSPG4-dependent migration in mandibular fibrochondrocytes using primary mandibular fibrochondrocytes isolated from control and full length NG2/CSPG4 knockout mice, in primary mandibular fibrochondrocytes isolated from NG2|DsRed reporter mice and in an immortalized mandibular fibrochondrocyte cell line with a mutated NG2/CSPG4 ectodomain. All three cells demonstrate similar results, with loss of the full length or truncated NG2/CSPG4 increasing the rate of cell migration in serum starvation/cell stress conditions. These findings clearly implicate NG2/CSPG4 as a key molecule in the regulation of cell migration in mandibular fibrochondrocytes in normal and cell stress conditions, underscoring the role of NG2/CSPG4 as a mechanosensitive signaling hub in the mandibular cartilage.
| S-EPMC10662293 | biostudies-literature
Project description:NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis
| PRJNA883722 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-12-02 | GSE245592 | GEO
Project description:Ischemic stroke is a serious medical condition that leads to neurological symptoms such as loss of motor and cognitive function. Focal cerebral ischemia (FCI) occurs due to interruption of blood supply to the site of injury, leading to the death of brain cells. Cells carrying Neural-glial antigen 2 (NG2) include glial cells serving primarily as olidogendrocyte precursors and a portion of pericytes. NG2 glia proliferate rapidly after ischemia and migrate to the site of injury, participate with astrocytes in glial scar formation, and contribute to the regeneration of the brain tissue. The ability of NG2 glia to differentiate into a different cell type than oligodendrocytes has been described but is still controversial. We therefore isolated NG2 cells and their derivatives labeled with tdTomato red fluorescent protein from the cortex of Rosa26-tdTomato/Cspg4-CreERT2 mice three days after middle cerebral artery occlusion (MCAO). Sham-operated animals were used as healthy controls (CTRL). We aimed to identify NG2 cell types and their derivatives in the cortex of healthy and ischemic mice and determine their incidence as well as characteristic gene expression.
2023-09-21 | E-MTAB-11967 | biostudies-arrayexpress