2. Academic Validation
  3. SEMA6D, Negatively Regulated by miR-7, Contributes to C28/I2 chondrocyte's Catabolic and Anabolic Activities via p38 Signaling Pathway

SEMA6D, Negatively Regulated by miR-7, Contributes to C28/I2 chondrocyte's Catabolic and Anabolic Activities via p38 Signaling Pathway

  • Oxid Med Cell Longev. 2022 Jun 16:2022:9674221. doi: 10.1155/2022/9674221.
Haoyu Yang 1,  Zhicheng Yang 2,  Zhentang Yu 2,  Chenwei Xiong 2,  Yi Zhang 2,  Junjie Zhang 2,  Yong Huang 2,  Xindie Zhou 2,  Jin Li 3,  Nanwei Xu 2
Affiliations

Affiliations

  • 1 Department of Orthopedics, Wuxi 9th People's Hospital Affiliated to Soochow University, Wuxi 214000, China.
  • 2 Department of Orthopedics, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou 213000, China.
  • 3 Department of Orthopedic Surgery, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314000, China.
PMID: 35757507 DOI: 10.1155/2022/9674221
Abstract

MiR-7 has been recognized as an osteoarthritis (OA-)-promoting factor, but the specific downstream pathway of miR-7 still remains unknown. Further investigation of the molecular regulatory mechanism of miR-7 might help develop a novel therapeutic method for OA. In this study, we revealed that Semaphorin 6D (SEMA6D) was a direct target gene of miR-7 and presented a negative regulatory relation with SEMA6D in vitro and in vivo. SEMA6D could improve OA in rat OA models, as indicated by H&E and Safranin O-Fast green staining, and also μCT analysis. Further evaluation of SEMA6D suggested that SEMA6D promotes the anabolism and reduces the catabolism of C28/I2 chondrocytes via inhibiting the activation of the p38 pathway. The present research illustrated that SEMA6D is a negatively regulatory factor of miR-7 and a pivotal mediator of catabolism and anabolism in C28/I2 chondrocytes. SEMA6D exerts its function via inhibiting the activation of the p38 pathway.

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