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

Author:

Yang Haoyu1,Yang Zhicheng2,Yu Zhentang2,Xiong Chenwei2,Zhang Yi2,Zhang Junjie2,Huang Yong2,Zhou Xindie2ORCID,Li Jin3ORCID,Xu Nanwei2

Affiliation:

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

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.

Funder

Jiaxing Science and Technology Project

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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