■软骨细胞活力,凋亡,骨性关节炎(OA)关节软骨损伤与迁移密切相关。外来体被鉴定为OA的潜在治疗剂。
■本研究旨在探讨骨细胞来源的外泌体在OA中的作用,特别关注它们对软骨修复和分子机制的影响。
■用IL-1β处理软骨细胞建立损伤细胞模型。软骨修复使用细胞计数试剂盒-8,流式细胞术,划痕试验,西方的Blot。使用定量实时PCR分析分子机制,生物信息学分析,西方的Blot。建立OA小鼠模型以探讨外泌体DLX2在体内的作用。
■骨细胞释放的外泌体促进细胞活力和迁移,并抑制细胞凋亡和细胞外基质(ECM)沉积。此外,外泌体上调DLX2表达,DLX2的敲除激活了Wnt通路。此外,外泌体通过传递DLX2减弱小鼠的OA。
■骨细胞来源的外泌体DLX2减轻了IL-1β诱导的软骨修复并使Wnt通路失活,从而缓解OA进展。研究结果表明,骨细胞来源的外泌体可能有望作为OA的治疗方法。
UNASSIGNED: Chondrocyte viability, apoptosis, and migration are closely related to cartilage injury in osteoarthritis (OA) joints. Exosomes are identified as potential therapeutic agents for OA.
UNASSIGNED: This study aimed to investigate the role of exosomes derived from osteocytes in OA, particularly focusing on their effects on cartilage repair and molecular mechanisms.
UNASSIGNED: An injury cell model was established by treating chondrocytes with IL-1β. Cartilage repair was evaluated using cell counting kit-8, flow cytometry, scratch test, and Western Blot. Molecular mechanisms were analyzed using quantitative real-time PCR, bioinformatic analysis, and Western Blot. An OA mouse model was established to explore the role of exosomal DLX2 in vivo.
UNASSIGNED: Osteocyte-released exosomes promoted cell viability and migration, and inhibited apoptosis and extracellular matrix (ECM) deposition. Moreover, exosomes upregulated DLX2 expression, and knockdown of DLX2 activated the Wnt pathway. Additionally, exosomes attenuated OA in mice by transmitting DLX2.
UNASSIGNED: Osteocyte-derived exosomal DLX2 alleviated IL-1β-induced cartilage repair and inactivated the Wnt pathway, thereby alleviating OA progression. The findings suggested that osteocyte-derived exosomes may hold promise as a treatment for OA.