Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading

Summary: Evidence indicates that mechanical loading plays an important role in osteoarthritis (OA) progression, while the specific pathological changes of the synovium under excessive mechanical loading are unclear. Results showed that excessive mechanical loading caused pro-inflammation of synovial...

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Main Authors: Wen Tang, Jian-bin Yin, Ren-gui Lin, Chun-yu Wu, Jia-luo Huang, Jin-jian Zhu, Ling-feng Yang, Guang-ming Li, Dao-zhang Cai, Liang-liang Liu, Yan-li Liu, Hai-yan Zhang
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Language:English
Published: Elsevier 2025-05-01
Series:iScience
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Online Access:http://www.sciencedirect.com/science/article/pii/S2589004225003918
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author Wen Tang
Jian-bin Yin
Ren-gui Lin
Chun-yu Wu
Jia-luo Huang
Jin-jian Zhu
Ling-feng Yang
Guang-ming Li
Dao-zhang Cai
Liang-liang Liu
Yan-li Liu
Hai-yan Zhang
author_facet Wen Tang
Jian-bin Yin
Ren-gui Lin
Chun-yu Wu
Jia-luo Huang
Jin-jian Zhu
Ling-feng Yang
Guang-ming Li
Dao-zhang Cai
Liang-liang Liu
Yan-li Liu
Hai-yan Zhang
author_sort Wen Tang
collection DOAJ
description Summary: Evidence indicates that mechanical loading plays an important role in osteoarthritis (OA) progression, while the specific pathological changes of the synovium under excessive mechanical loading are unclear. Results showed that excessive mechanical loading caused pro-inflammation of synovial macrophages, which has been confirmed to exist in OA. High Rapgef3 expression level was found in RNA sequencing of RAW246.7 subjected to 0.5 Hz and 20% cyclic tensile strain. We verified this in the synovium of patients with OA and destabilization of the medial meniscus (DMM)-OA mice. Interestingly, the Rapgef3 content of chondrocytes was very low. Primary chondrocytes treated with Rapgef3 alone did not show metabolic phenotype, but an OA phenotype appeared when treated with Rapgef3-stimulated macrophage culture supernatant. Mechanically, excessive mechanical loading activated p65-nuclear factor κB (NF-κB) pathway through Rapgef3, which promoted the inflammation of macrophage, resulting in severe articular cartilage injury. Intra-articular Rapgef3 knockout reversed synovitis and cartilage degeneration, which might provide a therapeutic target for OA.
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spelling doaj-art-861e22a671334dd29b24ed7cb6d7b5222025-08-20T03:09:03ZengElsevieriScience2589-00422025-05-0128511213110.1016/j.isci.2025.112131Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loadingWen Tang0Jian-bin Yin1Ren-gui Lin2Chun-yu Wu3Jia-luo Huang4Jin-jian Zhu5Ling-feng Yang6Guang-ming Li7Dao-zhang Cai8Liang-liang Liu9Yan-li Liu10Hai-yan Zhang11Department of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, ChinaDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, China; Corresponding authorThe Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, China; Corresponding authorDepartment of Joint Surgery, Center for Orthopaedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, China; Corresponding authorSummary: Evidence indicates that mechanical loading plays an important role in osteoarthritis (OA) progression, while the specific pathological changes of the synovium under excessive mechanical loading are unclear. Results showed that excessive mechanical loading caused pro-inflammation of synovial macrophages, which has been confirmed to exist in OA. High Rapgef3 expression level was found in RNA sequencing of RAW246.7 subjected to 0.5 Hz and 20% cyclic tensile strain. We verified this in the synovium of patients with OA and destabilization of the medial meniscus (DMM)-OA mice. Interestingly, the Rapgef3 content of chondrocytes was very low. Primary chondrocytes treated with Rapgef3 alone did not show metabolic phenotype, but an OA phenotype appeared when treated with Rapgef3-stimulated macrophage culture supernatant. Mechanically, excessive mechanical loading activated p65-nuclear factor κB (NF-κB) pathway through Rapgef3, which promoted the inflammation of macrophage, resulting in severe articular cartilage injury. Intra-articular Rapgef3 knockout reversed synovitis and cartilage degeneration, which might provide a therapeutic target for OA.http://www.sciencedirect.com/science/article/pii/S2589004225003918Biological sciencesMolecular biologyImmunologyBiomechanicsTranscriptomics
spellingShingle Wen Tang
Jian-bin Yin
Ren-gui Lin
Chun-yu Wu
Jia-luo Huang
Jin-jian Zhu
Ling-feng Yang
Guang-ming Li
Dao-zhang Cai
Liang-liang Liu
Yan-li Liu
Hai-yan Zhang
Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
iScience
Biological sciences
Molecular biology
Immunology
Biomechanics
Transcriptomics
title Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
title_full Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
title_fullStr Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
title_full_unstemmed Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
title_short Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
title_sort rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading
topic Biological sciences
Molecular biology
Immunology
Biomechanics
Transcriptomics
url http://www.sciencedirect.com/science/article/pii/S2589004225003918
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