Cytokine · 2025
Blocking Fpr3 ameliorates osteoarthritis by inhibiting NLRP3-mediated chondrocyte pyroptosis.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhou Bin, Huang Yaobin
Аннотация
OBJECTIVE: Osteoarthritis (OA) is a chronic joint disorder that frequently diagnosed in elderly individuals. While formyl peptide receptor 3 (Fpr3) is known to play a significant role in inflammation, its involvement in OA progression and chondrocyte pyroptosis remains unclear.
METHODS: Anterior cruciate ligament transection (ACLT) was used to create OA mouse model. Lipopolysaccharide (LPS) was utilized to induce inflammation in chondrocytes. We assessed the expression of Fpr3, chondrogenic markers (Collagen-II, SOX9, and Aggrecan), catabolic factors (MMP3, MMP13, and ADAMTS5), inflammatory cytokines (IL-1β, IL-18, and COX-2), and NLRP3 inflammasome members (NLRP3, ASC, Cleaved caspase1, and GSDMD-N) in cartilage from ACLT-induced mouse models and LPS-treated chondrocytes.
RESULTS: Fpr3 expression was significantly increased in both ACLT-induced OA mice and LPS-induced chondrocytes. Fpr3 knockdown reduced chondrocyte injury in OA mice. Fpr3 knockdown promoted the expression of collagen-II, SOX9, and aggrecan, while suppressing the expression of MMP3, MMP13, ADAMTS5, IL-1β, IL-18, COX-2, NLRP3, ASC, cleaved caspase1, and GSDMD-N in both experimental models.
CONCLUSIONS: Blocking Fpr3 ameliorated extracellular matrix degradation and pyroptosis during OA progress through the NLRP3 inflammasome. Modulating Fpr3 expression may be a therapeutic target for OA.
METHODS: Anterior cruciate ligament transection (ACLT) was used to create OA mouse model. Lipopolysaccharide (LPS) was utilized to induce inflammation in chondrocytes. We assessed the expression of Fpr3, chondrogenic markers (Collagen-II, SOX9, and Aggrecan), catabolic factors (MMP3, MMP13, and ADAMTS5), inflammatory cytokines (IL-1β, IL-18, and COX-2), and NLRP3 inflammasome members (NLRP3, ASC, Cleaved caspase1, and GSDMD-N) in cartilage from ACLT-induced mouse models and LPS-treated chondrocytes.
RESULTS: Fpr3 expression was significantly increased in both ACLT-induced OA mice and LPS-induced chondrocytes. Fpr3 knockdown reduced chondrocyte injury in OA mice. Fpr3 knockdown promoted the expression of collagen-II, SOX9, and aggrecan, while suppressing the expression of MMP3, MMP13, ADAMTS5, IL-1β, IL-18, COX-2, NLRP3, ASC, cleaved caspase1, and GSDMD-N in both experimental models.
CONCLUSIONS: Blocking Fpr3 ameliorated extracellular matrix degradation and pyroptosis during OA progress through the NLRP3 inflammasome. Modulating Fpr3 expression may be a therapeutic target for OA.