The novel-cell free bioactive formulation (BIOF2) modulates specific osteoarthritis’ detrimental and protective genes: A microarray analysis
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ABSTRACT:
PROVIDER: PRJNA694982 | ENA |
REPOSITORIES: ENA
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Project description:A novel-cell free bioactive formulation (BIOF2), US Patent No. 9669074B2, for arthrosic chondrocytes has been recently developed and proved as effective for treating severe knee osteoarthritis, we evaluated transcriptome changes in BIOF2-treated synovial fluid cells, isolated from patients with severe knee osteoarthritis to establish BIOF2 mechanism of action.
2021-01-27 | GSE165567 | GEO
Project description:Quantitative proteomics was used to find the protective effects of traditional Chinese medicine Epimedium, Salvia miltiorrhiza, and Dioscorea nipponica Makino against osteoarthritis.
2020-07-16 | PXD020396 |
Project description:TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy
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Project description:The severe and long-term consequences of traumatic brain injury (TBI) highlight the urgent need for effective neuroprotective therapies. Mesenchymal stromal cells (MSCs) show promise in TBI treatment through their secretome (conditioned media, CM). We previously identified a low-molecular-weight (<700Da) CM fraction with neuroprotective effects comparable to total CM after acute brain injury in vitro. Here we aimed at identifying key bioactive factors, reconstituting them into a synthetic cocktail (SYNT), and evaluating its efficacy in TBI models. Metabolomic profiling identified three prostaglandins and kynurenine, which were used to create SYNT. The SYNT formulation reduced cell death, neuronal damage, and induced protective gene expression changes (NeuN and BDNF upregulation, Cd11b and IL6 downregulation) after TBI in vitro. In vivo, SYNT conferred similar long-term functional benefits as CM, improving sensorimotor function up to 6 months and memory preservation at 4 months compared to saline-treated animals, thought, only CM reduced contusion volume at 5 months. Both treatments modulated neuroinflammation, evidenced by reduced microglial activation and astrogliosis in the pericontusional tissue at 6 months. These findings demonstrate the neuroprotective effects of MSC-secretome treatment in TBI and highlight prostaglandins and kynurenine as key mediators of this response. Our findings lay the groundwork for developing a standardized, cell-free therapeutic strategy for TBI based on MSC derivatives.
2025-06-18 | E-MTAB-14942 | biostudies-arrayexpress
Project description:Abnormal mechanical stress plays a crucial role in the progression of osteoarthritis (OA). However, more key factors regulating mechanical response remain to be explored. This study harvested temporomandibular joint synovium fluids from 96 patients and revealed that miR-330 is significantly reduced under abnormal mechanical stress. Similarly, the expression of miR-330 is also decreased in cartilage and subchondral bone tissue from clinical specimen and animal models. Global knock out of miR-330 aggravated osteoarthritis development in both temporomandibular joint and knee joint. Conditional knock out of miR-330 in either chondrocytes or osteoclasts exhibited similar phenotype in both mechanical instable and aging animal models, suggesting the importance of miR-330 in both types of cells. Further molecular mechanism exploration unveiled that miR-330 can regulate the catabolism of chondrocytes and osteoclasts via suppressing CTGF, FGFR1 and EPOR as well as key inflammatory cytokines such as IL-1β and TNF-α. More importantly, intra-articular supplement of miR-330 exerts a therapeutic effect by mitigating the detrimental impacts of abnormal mechanical stress, where inhibition of chondrocytes apoptosis, osteoclasts activation and inflammation were further confirmed via single-cell RNA sequencing analysis. In conclusion, this study for the first time revealed that miR-330 is a mechanical responsive, osteoarthritis protective micro RNA. We provide evidence that miR-330 has potential diagnostic and therapeutic value for both temporomandibular and knee osteoarthritis.
2026-06-11 | GSE307091 | GEO
Project description:Proctor2017- Role of microRNAs in osteoarthritis (miR140 in osteoarthritis)
This model is described in the article:
Computer simulation models
as a tool to investigate the role of microRNAs in
osteoarthritis.
Proctor CJ, Smith GR.
PLoS ONE 2017; 12(11): e0187568
Abstract:
The aim of this study was to show how computational models
can be used to increase our understanding of the role of
microRNAs in osteoarthritis (OA) using miR-140 as an example.
Bioinformatics analysis and experimental results from the
literature were used to create and calibrate models of gene
regulatory networks in OA involving miR-140 along with key
regulators such as NF-?B, SMAD3, and RUNX2. The individual
models were created with the modelling standard, Systems
Biology Markup Language, and integrated to examine the overall
effect of miR-140 on cartilage homeostasis. Down-regulation of
miR-140 may have either detrimental or protective effects for
cartilage, indicating that the role of miR-140 is complex.
Studies of individual networks in isolation may therefore lead
to different conclusions. This indicated the need to combine
the five chosen individual networks involving miR-140 into an
integrated model. This model suggests that the overall effect
of miR-140 is to change the response to an IL-1 stimulus from a
prolonged increase in matrix degrading enzymes to a pulse-like
response so that cartilage degradation is temporary. Our
current model can easily be modified and extended as more
experimental data become available about the role of miR-140 in
OA. In addition, networks of other microRNAs that are important
in OA could be incorporated. A fully integrated model could not
only aid our understanding of the mechanisms of microRNAs in
ageing cartilage but could also provide a useful tool to
investigate the effect of potential interventions to prevent
cartilage loss.
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To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
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| MODEL1705170005 | BioModels
Project description:Osteoarthritis (OA) features progressive cartilage loss with no effective regenerative therapies. This study investigated sturgeon cartilage peptides (SCPs) for OA repair and identified key bioactive peptides and mechanisms. SCPs, prepared by trypsin hydrolysis, were evaluated in in vitro and in vivo OA models. SCPs markedly improved cartilage damage, reduced matrix degradation, and increased chondrocyte proliferation to 126%.
2026-07-08 | GSE338020 | GEO
Project description:Osteoarthritis is a devastating disease of articular cartilage. The pathogenic factors contributing to this disorder are inflammation, extracellular matrix degradation and failure to rebuild the articular cartilage. Preclinical studies suggest that microRNA-140 (miR-140) may play a protective role in osteoarthritis development, but little is known about the mechanism by which this may occur. Here we present the results of overexpression of miR-140 in an in vitro model of osteoarthritis, evaluated by global proteomics analysis. We show that inflammation is reduced through the differential synthesis of multiple proteins involved in the nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NFKB) pathway, articular cartilage regeneration may be induced through the upregulation of many of the components involved in the synthesis of hyaline extracellular matrix, and cartilage degeneration may be reduced through the reduced expression of aggrecanases. Thus, miR-140 overexpression may have a beneficial effect on the development of osteoarthritis through the differential synthesis of a surprisingly large number of proteins involved in all three pathogenic processes. These results show how intraarticular injection of miR-140 may benefit patients suffering from osteoarthritis.
2018-10-26 | PXD003362 | Pride
Project description:Bioactive RNA in Maternal Breastmilk
| PRJNA791909 | ENA
Project description:To further explain pathology of mTORC1 -stimulated osteoarthritis, we have employed whole genome microarray expression profiling as a discovery platform to identify miRNAs which involved in development of mTORC1-stimulated osteoarthritis We generated Col2a1-specific deletion of Tsc1 mice. mTORC1 induced miRNAs expression in development of osteoarthritis was measured at eight weeks after birth. Independent experiments were performed using knee joint cartilage from Col2a1Tsc1KO and control mice.
2016-07-30 | E-GEOD-71484 | biostudies-arrayexpress