Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1224406 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32375983_1.fastq.gz | Fastqsanger.gz | |||
| SRR32375983_2.fastq.gz | Fastqsanger.gz | |||
| SRR32375984_1.fastq.gz | Fastqsanger.gz | |||
| SRR32375984_2.fastq.gz | Fastqsanger.gz | |||
| SRR32375985_1.fastq.gz | Fastqsanger.gz |
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Project description:Although our data is providing the evidence that Ihh regulates nasal and mandibular cartilage development to establish facial and masticatory system, the cartilage gene network conducted by Ihh signaling has not been broadly investigated. To establish such gene expression profile, we selected mandibular condylar cartilage to examine differentiating cartilage tissue. The cartilage histologically indicates simple endochondral ossification and mutant sections positive to Tomato staining presented decreased and disrupted cartilage.
2020-03-29 | GSE134768 | 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:Background Extracellular matrix (ECM) protein malfunction or defect may lead to temporomandibular joint osteoarthritis (TMJ OA). Dentin sialophophoprotein (DSPP) is a mandibular condylar cartilage ECM protein, and its deletion impacted cell proliferation and other extracellular matrix alterations of postnatal condylar cartilage. However, it remains unclear if long-term loss of function of DSPP leads to TMJ OA. The study aimed to test the hypothesis that long-term haploinsufficiency of DSPP causes TMJ OA. Materials and Methods To determine whether Dspp+/- mice exhibit TMJ OA but no severe tooth defects, mandibles of wild-type (WT), Dspp+/-, and Dspp homozygous (Dspp-/-) mice were analyzed by Micro-computed tomography (micro-CT). To characterize the progression and possible mechanisms of osteoarthritic degeneration over time in Dspp+/- mice over time, condyles of Dspp+/- and WT mice were analyzed radiologically, histologically, and immunohistochemically. Results Micro-CT and histomorphometric analyses revealed that Dspp+/- and Dspp-/- mice had significantly lower subchondral bone mass, bone volume fraction, bone mineral density, and trabecular thickness compared to WT mice at 12 months. Interestingly, in contrast to Dspp-/- mice which exhibited tooth loss, Dspp+/- mice had minor tooth defects. RNA sequencing data showed that haplodeficency of DSPP affects the biological process of ossification and osteoclast differentiation. Additionally, histological analysis showed that Dspp+/- mice had condylar cartilage fissures, reduced cartilage thickness, decreased articular cell numbers and severe subchondral bone cavities, and with signs that were exaggerated with age. Radiographic data showed an increase in subchondral osteoporosis up to 18 months and osteophyte formation at 21 months. Moreover, Dspp+/- mice showed increased distribution of osteoclast in the subchondal bone and increased expression of MMP2, IL-6, FN-1, and TLR4 in the mandibular condylar cartilage. Conclusions Dspp+/- mice exhibit TMJ OA in a time-dependent manner, with lesions in the mandibular condyle attributed to hypomineralization of subchondral bone and breakdown of the mandibular condylar cartilage, accompanied by upregulation of inflammatory markers.
2024-03-19 | GSE261528 | GEO
Project description:Understanding the effects of biomechanical loading on human growth plate cartilage, which are unknown so far, could uncover diagnostic and therapeutic avenues. To address this, we used rare human growth plate biopsies obtained from children undergoing epiphysiodesis. These biopsies were exposed to a precisely controlled mechanical loading application using a microloading device. Subsequently, the biopsies were cultured for 24 hours post-mechanical loading, followed by RNA-sequencing analyses to decipher the molecular responses.
2024-12-18 | GSE246390 | GEO
Project description:Mechanical loading and gene expression - Microarray study
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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.
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
Project description:Temporomandibular joint degenerative disease (TMJ-DD) is a chronic form of TMJ disorder that specifically afflicts people over the age of 40 and targets women at a higher rate than men. Prevalence of TMJ-DD in this population suggests that estrogen loss plays a role in the disease pathogenesis. Thus, the goal of the present study was to determine the role of estrogen on chondrogenesis and homeostasis via estrogen receptor alpha (ERα) during growth and maturity of the joint. Young and mature WT and ERαKO female mice were subjected to ovariectomy procedures and then given placebo or estradiol treatment. The effect of estrogen via ERα on fibrocartilage morphology, matrix production, and protease activity was assessed. In the young mice, estrogen via ERα promoted mandibular condylar fibrocartilage chondrogenesis partly by inhibiting the canonical Wnt signaling pathway through upregulation of sclerostin (Sost). In the mature mice, protease activity was partly inhibited with estrogen treatment via the upregulation and activity of protease inhibitor 15 (Pi15) and alpha-2-macroglobulin (A2m). The results from this work provide a mechanistic understanding of estradiol on TMJ growth and homeostasis and can be utilized for development of therapeutic targets to promote regeneration and inhibit degeneration of the mandibular condylar fibrocartilage.
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