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Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from osteocyte-enriched subchondral bone]

ABSTRACT: Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from osteocyte-enriched subchondral bone]

PROVIDER: PRJNA1198879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31732170.fastq.gz	Fastqsanger.gz
	SRR31732171.fastq.gz	Fastqsanger.gz
	SRR31732172.fastq.gz	Fastqsanger.gz
	SRR31732173.fastq.gz	Fastqsanger.gz
	SRR31732174.fastq.gz	Fastqsanger.gz

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Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from osteocyte-enriched subchondral bone]

Project description:Osteoarthritis (OA) is the most common degenerative joint disease. During its initiation and early progression a disruption in subchondral bone (SCB) remodeling, induced by excessive and cumulative mechanical loading, occurs before cartilage degeneration. While it is known that osteocytes in the SCB are mainly responsible for mechanosensing, their role in the early phases of OA are still unclear. Here, we found that mechanical stress induces SCB osteocytes to secrete extracellular vesicles (EVs) that accelerate cartilage metabolic dysregulation. By gain- and loss-of function experiments we show that such EVs via miR-23b-3p promote cartilage catabolism while inhibiting their anabolism. Mechanistically, miR-23b-3p inhibits mitophagy by targeting OTUD4 to promote this metabolic skewing. Further, by inhibiting miR-23b-3p in either osteocytes or chondrocytes we could alleviate cartilage degeneration and OA progression in a mouse model. Together, our findings show that SCB osteocytes communicate with chondrocytes via EVs and that targeting a key EV-derived miRNA can ameliorate OA progression.

2025-04-12 | GSE284359 | GEO

Targeting long non-coding RNA H19 in Subchondral Bone Osteocytes Alleviates Cartilage Degradation in Osteoarthritis

Project description:Introduction: Emerging evidence suggests long non-coding RNA (lncRNA) H19 is associated with osteoarthritis (OA) pathology. However, how H19 contributes to OA has not been reported. This study aims to investigate the biological function of H19 in OA subchondral bone remodeling and OA progression. Methods: Clinical joint samples and OA animal models induced by medial meniscus destabilization (DMM) surgery were used to verify the causal relationship between osteocyte H19 and OA subchondral bone and cartilage changes. MLO-Y4 osteocyte cells subjected to fluid shear stress were used to verify the mechanism underlying H19-mediated mechano-response. Finally, the antisense oligonucleotide (ASO) against H19 was delivered to mice knee joints by magnetic metal-organic framework (MMOF) nanoparticles in order to develop a site-specific delivery method for targeting osteocyte H19 for OA treatment. Results: Both clinical OA subchondral bone and wildtype mice with DMM-induced OA exhibit aberrant higher subchondral bone mass with more H19 expressing osteocytes. On the contrary, osteocyte-specific deletion of H19 mice is less vulnerable to DMM-induced OA phenotype. In MLO-Y4 cells, H19-mediated osteocyte mechano-response through PI3K/AKT/GSK3 signals activation by EZH2-induced H3K27me3 regulation on PP2A inhibition. Targeted inhibition of H19 (using ASO-loaded MMOF) substantially alleviates subchondral bone remodeling and OA phenotype. Discussion: In summary, our results provide new evidence that the elevated H19 expression in osteocytes may contribute to aberrant subchondral bone remodeling and OA progression. H19 appears to be required for the osteocyte response to mechanical stimulation, and targeting H19 represents a new promising approach for OA treatment.

2025-03-05 | GSE254053 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only osteocyte-enriched subchondral bone]

2025-04-12 | GSE284357 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only osteocyte-enriched subchondral bone]

Project description:Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only osteocyte-enriched subchondral bone]

| PRJNA1198876 | ENA

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from plasma]

2025-04-12 | GSE284361 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [primary chondrocytes]

2025-04-12 | GSE284358 | GEO

Targeting osteoblastic Mig6-EGFR signaling ameliorates osteoarthritis progression via inhibiting aberrant subchondral bone remodeling

Project description:Aberrant subchondral bone remodeling is a critical factor in osteoarthritis (OA) pathogenesis. We observed significant downregulation of Mitogen-induced gene-6 (Mig6) and upregulation of EGFR phosphorylation in subchondral bone osteoblasts, strongly correlating with OA severity in human and animal models. Mig6 is the most important factor mediating mechanical stress-activated EGFR, which inhibits osteogenic activity and modulates mechano-responsiveness. Osteoblast-specific Mig6 deletion exacerbated OA progression by promoting subchondral bone remodeling, whereas gefitinib-mediated inhibition of EGFR phosphorylation attenuated OA symptoms in mice, rats, and Mig6 knockout rats. Furthermore, loss of osteoblastic Mig6 disrupted the subchondral bone microenvironment, increasing inflammation, angiogenesis, and neuronal activity. Mechanistically, aberrant mechanical loading downregulated Mig6, activating phosphorylation of EGFR and the downstream JAK-STAT3 pathway, thereby promoting subchondral bone remodeling and accelerating OA progression. These findings reveal a novel mechanism by which osteoblastic Mig6 regulates subchondral bone remodeling in OA, highlighting Mig6 as a potential therapeutic target.

2025-07-31 | GSE302025 | GEO

Genome-wide Expression Profiles of Subchondral Bone in Osteoarthritis

2013-10-24 | GSE51588 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from plasma]

Project description:Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from plasma]

| PRJNA1198886 | ENA

Genome-wide Expression Profiles of Subchondral Bone in Osteoarthritis

Project description:To date, all of the prior osteoarthritic microarray studies in human tissue have focused on the overlying articular cartilage, meniscus, or synovium but not the underlying subchondral bone. In our previous study, our group developed a methodology for high quality RNA isolation from site-matched cartilage and bone from human knee joints, which allowed us to perform candidate gene expression analysis on the subchohndral bone (published on Osteoarthritis and Cartilage on Dec/5/2012 (doi: 10.1016/j.joca.2012.11.016). To the best of our knowledge, the current study is the first to successfully perform whole-genome microarray profiling analyses of human osteoarthritic subchondral bone. We believe our comprehensive microarray results can improve the understanding of the pathogenesis of osteoarthritis and could further contribute to the development of new biomarker and therapeutic strategies in osteoarthritis. Following histological assessment of the integrity of overlying cartilage and the severity of bone abnormality by microcomputed tomography, we isolated total RNA from regions of interest from human OA (n=20) and non-OA (n=5) knee lateral and medial tibial plateaus (LT and MT). A whole-genome profiling study was performed on an Agilent microarray platform and analyzed using Agilent GeneSpring GX11.5. Confirmatory quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis was performed on samples from nine OA individuals to confirm differential expression of 85 genes identified by microarray. Ingenuity Pathway Analysis (IPA) was used to investigate canonical pathways and immunohistochemical staining was performed to validate protein expression levels in samples.

2013-10-24 | E-GEOD-51588 | biostudies-arrayexpress

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