周期性循环机械张力诱导的终板软骨细胞衰老和退变中 YAP1 的作用机制。
Mechanism of YAP1 in the senescence and degeneration of endplate chondrocytes induced by intermittent cyclic mechanical tension.
机构信息
Division of Life Science and Medicine, Department of Orthopedic, The First Affiliated Hospital of USTC, University of Science and Technology of China, HeFei, 230001, Anhui, China.
Division of Life Science and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, HeFei, 230001, Anhui, China.
出版信息
J Orthop Surg Res. 2023 Mar 22;18(1):229. doi: 10.1186/s13018-023-03704-w.
BACKGROUND
This study aimed to investigate the potential mechanism of YAP1 in the senescence and degeneration of endplate chondrocytes induced by intermittent cyclic mechanical tension (ICMT).
METHODS
According to the Pfirrmann grade evaluation classification, 30 human endplate cartilage tissues were divided into the lumbar vertebra fracture (LVF) group and lumbar disc herniation (LDH) group. Then, quantitative reverse transcription polymerase chain reaction, western blot, flow cytometry, hematoxylin-eosin staining, and senescence-associated β-galactosidase staining were performed. The difference in extracellular matrix expression between LVF and LDH endplate cartilage was detected. Second, the effect of ICMT on endplate chondrocytes degeneration was observed. Finally, the key regulatory role of YAP1 in ICMT-induced endplate cartilage degeneration was further verified.
RESULTS
In degraded human endplate cartilage and tension-induced degraded endplate chondrocytes, the expression of YAP1, COL-2A, and Sox9 was decreased. Conversely, the expression of p53 and p21 was increased. By regulating YAP1 in vivo and in vitro, we can achieve alleviation of ICMT-induced senescence of endplate chondrocytes and effective treatment of disc degeneration.
CONCLUSIONS
ICMT could induce senescence and degeneration of endplate chondrocytes, and ICMT-induced senescence and degeneration of endplate chondrocytes could be alleviated by regulating YAP1 expression.
背景
本研究旨在探讨 YAP1 在间歇性循环机械张力（ICMT）诱导的终板软骨细胞衰老和退变中的潜在机制。
方法
根据 Pfirrmann 分级评估分类，将 30 个人类终板软骨组织分为腰椎骨折（LVF）组和腰椎间盘突出症（LDH）组。然后，进行定量逆转录聚合酶链反应、western blot、流式细胞术、苏木精-伊红染色和衰老相关β-半乳糖苷酶染色，以检测 LVF 和 LDH 终板软骨之间细胞外基质表达的差异。其次，观察 ICMT 对终板软骨细胞退变的影响。最后，进一步验证 YAP1 在 ICMT 诱导的终板软骨退变中的关键调节作用。
结果
在降解的人终板软骨和张力诱导的降解终板软骨细胞中，YAP1、COL-2A 和 Sox9 的表达减少，而 p53 和 p21 的表达增加。通过体内和体外调节 YAP1，可以减轻 ICMT 诱导的终板软骨细胞衰老，并有效治疗椎间盘退变。
结论
ICMT 可诱导终板软骨细胞衰老和退变，通过调节 YAP1 的表达可以减轻 ICMT 诱导的终板软骨细胞衰老和退变。
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