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  2. BMP5 silencing inhibits chondrocyte senescence and apoptosis as well as osteoarthritis progression in mice

BMP5 silencing inhibits chondrocyte senescence and apoptosis as well as osteoarthritis progression in mice

  • Aging (Albany NY). 2021 Mar 19;13(7):9646-9664. doi: 10.18632/aging.202708.
Yan Shao 1 2 3 Chang Zhao 1 2 3 Jianying Pan 1 2 3 Chun Zeng 1 2 3 Hongbo Zhang 1 2 3 Liangliang Liu 1 2 3 Kai Fan 1 2 3 Xin Liu 1 2 3 Bingsheng Luo 1 2 3 Hang Fang 1 2 3 Xiaochun Bai 1 2 3 Haiyan Zhang 1 2 3 Daozhang Cai 1 2 3
Affiliations

Affiliations

  • 1 Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
  • 2 The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China.
  • 3 Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, China.
Abstract

In this study, we using the in vivo destabilization of the medial meniscus (DMM) mouse model to investigate the role of Bone Morphogenetic Protein 5 (BMP5) in osteoarthritis (OA) progression mediated via chondrocyte senescence and Apoptosis. BMP5 expression was significantly higher in knee articular cartilage tissues of OA patients and DMM model mice than the corresponding controls. The Osteoarthritis Research Society International scores based on histological staining of knee articular cartilage sections were lower in DMM mice where BMP5 was knocked down in chondrocytes than the corresponding controls 4 weeks after DMM surgery. DMM mice with BMP5-deficient chondrocytes showed reduced levels of matrix-degrading enzymes such as MMP13 and ADAMTS5 as well as reduced cartilage destruction. BMP5 knockdown also decreased chondrocyte Apoptosis and senescence by suppressing the activation of p38 and ERK MAP kinases. These findings demonstrate that BMP5 silencing inhibits chondrocyte senescence and Apoptosis as well as OA progression by downregulating activity in the p38/ERK signaling pathway.

Keywords

BMP5; chondrocyte; osteoarthritis; p38/ERK; senescence.

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