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Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis

机译:血管内皮细胞分泌的外泌体通过促进软骨细胞凋亡来促进骨关节炎发病机制

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摘要

Exosomes are major mediators of cell-to-cell communication, and are involved in many physiological and pathological processes. Recently, the roles of exosomes in osteoarthritis (OA) and their therapeutic potential have received increasing attention. Exosomes derived from vascular endothelial cells have been confirmed to participate in the occurrence and development of numerous diseases; however, their effects in OA have not been reported. Here, we demonstrated the roles of exosomes secreted by vascular endothelial cells in the development of OA. Through in vivo and in vitro experiments, we demonstrated that exosomes derived from vascular endothelial cells decreased the ability of chondrocytes to resist oxidative stress by inhibiting autophagy and p21 expression, thereby increasing the cellular ROS content and inducing apoptosis. These findings indicate that exosomes derived from vascular endothelial cells promote the progression of OA, thus, providing new ideas for the diagnosis and treatment of OA.
机译:外泌体是细胞对细胞通信的主要介质,并且参与许多生理和病理过程。最近,外来体在骨关节炎(OA)中的作用及其治疗潜力已经增加了越来越关注。已经证实源自血管内皮细胞的外泌体参与了许多疾病的发生和发展;但是,他们在OA中的影响尚未报告。在这里,我们证明了外泌体分泌的血管内皮细胞在OA的发育中的作用。通过体内和体外实验,我们证明源自血管内皮细胞的外泌体降低了通过抑制自噬和P21表达来抵抗氧化应激的软骨细胞的能力,从而增加了细胞ROS含量和诱导细胞凋亡。这些发现表明,来自血管内皮细胞的外来源性促进了OA的进展,从而为OA的诊断和治疗提供了新的思路。

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