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Osteocyte-specific deletion of Gasdermin D drives osteoarthritis cartilage degeneration by promoting inflammation and remodeling in subchondral bone.

ABSTRACT: In osteoarthritis, we discovered that pyroptosis of osteocytes in the subchondral bone contributes to disease progression. Ongoing studies using knockout mouse models aim to elucidate the effects of inhibiting this pathological pathway on disease progression .

ORGANISM(S): Mus musculus

PROVIDER: GSE301329 | GEO | 2026/06/15

REPOSITORIES: GEO

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Osteocyte-specific deletion of Gasdermin D drives osteoarthritis cartilage degeneration by promoting inflammation and remodeling in subchondral bone

Project description:In osteoarthritis, we discovered that the number of osteocytes in the subchondral bone is reduced. By investigating the interaction between chondrocytes and osteocytes, we aim to elucidate the underlying pathological mechanisms.

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Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only 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.

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

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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.

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

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Osteocyte Parvalbumin Mediates Mechanotransduction to Attenuate Osteoarthritis

Project description:Osteoarthritis (OA) is a leading cause of disability among the elderly, characterized by aberrant subchondral bone remodeling that precedes cartilage degeneration. We identify parvalbumin (Pvalb) in osteocytes as a critical mechanosensory regulator of this pathological process. Pvalb expression is significantly reduced in osteocytes from both OA patients and male murine models of the disease. Conditional deletion of Pvalb in osteocytes accelerates OA progression, whereas bone-targeted restoration of Pvalb expression mitigates disease manifestations. Mechanistically, Pvalb maintains calcium homeostasis by competing with CaMKIV for calmodulin binding. Under excessive mechanical loading, Pvalb expression is suppressed, leading to activation of the Ca²+-CaMKIV-CREB signaling pathway, increased RANKL production, and subsequent osteoclast activation and pathological bone remodeling. These findings identifies an osteocyte-mediated mechanotransduction pathway in OA pathogenesis and underscore Pvalb as a promising therapeutic target.

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Osteocyte Parvalbumin Mediates Mechanotransduction to Attenuate Osteoarthritis

| PXD079252 |

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.

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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

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