Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sequencing of the effect of mechanical stimulation on mesenchymal stem cells

ABSTRACT: Mechanical force is a crucial external stimulus that plays a significant role in regulating bone structure and remodeling. Excessive loading of the bone and joint can lead to increased catabolism, chondrocyte necrosis, apoptosis and damage to the collagen network of bone(3–5). Osteoarthritis (OA), a degenerative osteoarticular disease, is associated with abnormal mechanical force stimulation, which can occur in various joints such as knee, temporomandibular joint [TMJ], shoulder and hip(6). Conversely, the absence of mechanical loading, such as prolonged bed rest or exposure to a microgravity environment in space, can result in a rapid decrease in bone mass and strength. Understanding how mechanical stimuli regulate bone homeostasis is crucial for exploring therapeutic strategies for bone metabolic diseases.Mesechymal stem cells (MSCs) act as the external force sensoring and compression-bearing elements.What we want to explore is how mechanical stimulation affects the genome changes of mesenchymal stem cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE247273 | GEO | 2023/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effects of mechanical stress and deficiency of dihydrotestosterone or 17β-estradiol on temporomandibular joint osteoarthritis in mice

Project description:Temporomandibular joint osteoarthritis (TMJ-OA), a subtype of temporomandibular joint dysfunction (TMD), is characterized by progressive cartilage degradation, subchondral bone erosion, and chronic pain. Although there has been extensive research on TMJ-OA, its etiology remains unknown. Age, hormonal factors, and excessive mechanical stress on the TMJ are proposed risk factors for TMJ-OA. Using microarrays, we discovered two disease susceptibility genes that have been suggested to be involved in the pathogenic mechanism of TMJ-OA.

2020-09-18 | GSE158106 | GEO

NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis

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

Mechanical force promotes dimethylarginine dimethylaminohydrolase 1-mediated hydrolysis of the metabolite asymmetric dimethylarginine to enhance bone formation

Project description:<p>Mechanical force is critical for the development and remodeling of bone. Here we report that mechanical force regulates the production of the metabolite asymmetric dimethylarginine (ADMA) via regulating the hydrolytic enzyme dimethylarginine dimethylaminohydrolase 1 (Ddah1) expression in osteoblasts. The presence of -394 4N del/ins polymorphism of Ddah1 and higher serum ADMA concentration are negatively associated with bone mineral density. Global or osteoblast-specific deletion of Ddah1 leads to increased ADMA level but reduced bone formation. Further molecular study unveils that mechanical stimulation enhances TAZ/SMAD4-induced Ddah1 transcription. Deletion of Ddah1 in osteoblast-lineage cells fails to respond to mechanical stimulus-associated bone formation. Taken together, the study reveals mechanical force is capable of down-regulating ADMA to enhance bone formation.</p>

2021-11-23 | MTBLS3725 | MetaboLights

Transcription profiling of mouse embryonic E16.5 temporomandibular joint

Project description:We conducted a genetic analysis of the developing temporo-mandibular joint (TMJ), a highly specialized synovial joint that permits movement and function of the mammalian jaw. First, we used laser capture microdissection to perform a genome-wide expression analysis of each of its developing components. The expression patterns of genes identified in this screen were examined in the TMJ and compared to other synovial joints including the shoulder joint and the hip joint. Striking differences were noted, indicating that the TMJ forms via a distinct molecular program. Several components of the Hedgehog (Hh) signaling pathway are among the genes identified in the screen, including Gli2, which is expressed specifically in the condyle and in the disk of the developing TMJ. We found that mice deficient in Gli2 display aberrant TMJ development such that the condyle loses its growth plate-like cellular organization and no disk is formed. In addition, we utilized a conditional strategy to remove activity of the Hh co-receptor encoded by Smo from chondrocyte progenitors. This cell autonomous loss of Hh signaling allows for disk formation, but the resulting structure fails to separate from the condyle. Thus, these experiments establish that Hh signaling acts at two distinct steps in disk morphogenesis, condyle initiation and disk-condyle separation, and provide a molecular framework for future studies of the TMJ. Experiment Overall Design: Mouse embryos fresh frozen and TMJ tissue captured by LCM. 3 samples in biological triplicate.

2009-10-23 | E-GEOD-17473 | biostudies-arrayexpress

Expression data of wild type and DDR-1-KO mice TMJ-cartilage

Project description:The discoidin domain receptor 1 (DDR-1) deficient mice exhibit a high incidence of osteoarthritis (OA) in the temporomandibular joint (TMJ) already at early age. Young DDR-1 knock-out mice show typical histological signs of OA, like, surface fissures, loss of proteoglycans, cluster formation of the chondrocytes, altered collagen types as well as atypical arrangement of the collagen fibrils. The isolated chondrocytes from the TMJ exhibit an osteoarthritic character with high amounts of Runt-related transcription factor 2 (runx-2) and collagen type I compared to low levels of SRY (sex determining region Y)-box 9 (sox-9) and aggrecan. Especially, the amount of discoidin domain receptor 2 (DDR2) is increased, which is key player of OA in this model. The gene expression as well as the proteins of the DDR-1-deficient chondrocytes from the TMJ could be influenced by a three dimensional matrix, combined with a knockdown of runx-2 or the stimulation with components of the extracellular matrix, for example nidogen-2. These manipulations caused the osteoarthritic chondrocytes of DDR-1-deficient mice to change their gene expression towards a signature of more physiological cartilage and will open new possibilities for future regenerative treatment options of temporomandibular disorders like OA of the TMJ.

2012-01-25 | GSE35297 | GEO

Unilateral mastication induced alternations of microRNAs expression profiling in synovium of rat temporomandibular joint

Project description:The present study investigated the alterations of miRNA expression profiling in synovium of temporomandibular joint(TMJ) in a rat model of experimental unilateral mastication. The synovium tissue of TMJ condyles from rats with 4- and 8-weeks unilateral mastication were harvested to extract miRNA for profiling holistic expression alternations. A total of 20 differentially expressed miRNAs were identified. Except for 3 miRNAs with uncertain function, those miRNAs are associated with cell proliferation, invasion, and osteoblast differentiation process.

2018-05-16 | GSE114499 | GEO

RNA expression data of embryonic E16.5 mouse temporomandibular joint (TMJ)

2009-10-15 | GSE17473 | GEO

Mus musculus

Project description:RNA expression data of embryonic E16.5 mouse temporomandibular joint (TMJ)

| PRJNA118717 | ENA

Mechanical loading and gene expression - Microarray study

Project description:Skeletal integrity in humans and animals is maintained by daily mechanical loading. It has been widely accepted that osteocytes function as mechanosensors. Many biochemical signaling molecules are involved in the response of osteocytes to mechanical stimulation. The aim of this study was to identify genes involved in the translation of mechanical stimuli into bone formation. The four-point bending model was used to induce a single period of mechanical loading (comprising 300 cycles (2 Hz) using a peak magnitude of 60 N) on the right tibia, while the contra lateral left tibia served as control. Six hours after loading, the effects of mechanical loading on gene-expression were determined with microarray analysis. Protein expression of differentially regulated genes was evaluated with immunohistochemistry. Nine genes were found to exhibit a significant differential gene expression in LOAD compared to control. MEPE, Garnl1, V2R2B, and QFG TN1 olfactory receptor were up-regulated, and creatine kinase (muscle form), fibrinogen-B beta-polypeptide, monoamine oxidase A, troponin-C and kinesin light chain-C were down-regulated. Validation with real-time RT-PCR analysis confirmed the up regulation of MEPE and the down-regulation of creatine kinase (muscle form) and troponin-C in the loaded tibia. Immunohistochemistry showed that the increase of MEPE protein expression was already detectable six hours after mechanical loading. In conclusion, these genes probably play a role during translation of mechanical stimuli six hours after mechanical loading. The modulation of MEPE expression may indicate a connection between bone mineralization and bone formation after mechanical stimulation. Two groups: LOAD vs contralateral control and SHAM vs contralateral control (n=5/group)

2013-11-21 | E-GEOD-50707 | biostudies-arrayexpress

Mechanical loading and gene expression - Microarray study

2013-11-21 | GSE50707 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data