Scholarlink

<p>Excessive mechanical loading leads to cartilage degeneration. However, short-term responses of the synovium and cartilage to overloading and interactions between these tissues remain poorly understood. We developed a mouse model to study excessive mechanical loading, combining treadmill exercise with weight attachment. Time-course RNA sequencing of the synovium and cartilage displayed transient upregulation of inflammation after single overloading, whereas it was prolonged by repeated overloading. Ingenuity pathway analysis identified <i>Inhba</i>, encoding inhibin subunit beta A, as an upstream molecule for the cartilage transcriptomic changes. <i>Inhba</i> was highly induced by single or repeated overloading in the synovium, and Inhba protein was detected in the superficial layer of the synovium. Supplementation with recombinant activin A, a homodimer of Inhba, exerted catabolic effects in mouse primary chondrocytes. Further insights into mechano-responses of the synovium and cartilage, including the role played by Inhba in the synovium–cartilage interaction, may contribute to the elucidation of osteoarthritis pathogenesis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Short-term overloading exercise attenuates articular chondrocyte features partly via synovium–cartilage interactions mediated by inhibin subunit beta A

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年2月25日

查看全文
  • Yusuke Arino,
  • Asuka Terashima,
  • Toshiya Tsubaki,
  • Yasuhide Iwanaga,
  • Yasunori Omata,
  • Sakae Tanaka,
  • Taku Saito

摘要

Excessive mechanical loading leads to cartilage degeneration. However, short-term responses of the synovium and cartilage to overloading and interactions between these tissues remain poorly understood. We developed a mouse model to study excessive mechanical loading, combining treadmill exercise with weight attachment. Time-course RNA sequencing of the synovium and cartilage displayed transient upregulation of inflammation after single overloading, whereas it was prolonged by repeated overloading. Ingenuity pathway analysis identified Inhba, encoding inhibin subunit beta A, as an upstream molecule for the cartilage transcriptomic changes. Inhba was highly induced by single or repeated overloading in the synovium, and Inhba protein was detected in the superficial layer of the synovium. Supplementation with recombinant activin A, a homodimer of Inhba, exerted catabolic effects in mouse primary chondrocytes. Further insights into mechano-responses of the synovium and cartilage, including the role played by Inhba in the synovium–cartilage interaction, may contribute to the elucidation of osteoarthritis pathogenesis.