Table 1 The exosomes from different joint cells and their biological actions on the target cells
From: Exosomes: roles and therapeutic potential in osteoarthritis
Tissue | Cell type | Separation method | Exosome diameter | Target cells | Biological effects | Mechanisms of actions |
|---|---|---|---|---|---|---|
Cartilage | Human OA chondrocytes | Precipitation | – | Chondrocytes | Inhibit chondrocytes proliferation and promote the apoptosis of chondrocytes. | GSK-3β-mediated regulation of HULC and miR-372-3p in exosomes.110 |
Cartilage | Mouse primary chondrocytes | Ultracentrifugation | 40–110 nm | Chondrocytes and macrophages | Restore mitochondrial dysfunction and polarize macrophage response toward an M2 phenotype. | The restoration of normal mitochondrial structure and moderate ROS production.106 |
Cartilage | Human OA chondrocytes | Ultracentrifugation and Size-based filtration | 30–150 nm | Macrophages | Stimulate inflammasome activation and increase IL-1β production. | Inhibit ATG4B expression via miR-449a-5p, which leading to inhibition of autophagy in LPS-primed macrophages.107 |
Cartilage | Rabbit articular chondrocytes | Size-based filtration | 30–200 nm | Chondrocyte-progenitor cells (CPCs) | Promotes ectopic chondrogenesis and inhibiting angiogenesis. | Stimulate CPCs proliferation and increase the expression of chondrogenesis markers.108 |
Cartilage | Chondrocytes (cell line) | Ultracentrifugation | Bone marrow mesenchymal stem cells (BMSCs) | Promote chondrogenic differentiation of BMSCs | Activate Wnt/b-catenin pathways via targeting GSK-3b by exosomal miR-8485.111 | |
Cartilage | MiR‐95‐5p‐overexpressing chondrocytes | Ultracentrifugation | 90–150 nm | Chondrocytes | Regulate cartilage development in hMSCs during chondrogenesis and promote cartilage matrix expression. | Inhibit histone deacetylase 2/8 expression via MiR‐95‐5p.109 |
Synovial tissue | IL-1β-stimulated synovial fibroblasts | Ultracentrifugation and precipitation | 40-100 nm | Articular chondrocytes | Induce OA-like changes both in vitro and in ex vivo models. | Upregulate MMP-13 and ADAMTS-5 expression and down-regulate COL2A1 and ACAN in chondrocytes.121 |
Synovial tissue | MiR-140-5p-overexpressing human synovial mesenchymal stem cells | Affinity-Based capture | 30–150 nm | Articular chondrocytes | Enhance proliferation and migration of chondrocytes without decreasing ECM secretion in vitro Promote cartilage regeneration and maintain cartilage matrix content in vivo | Wnt5a and Wnt5b carried by exosomes to activate Wnt/YAP signaling pathway MiR-140-5p-mediated inhibition of RalA and increase of SOX9 and Aggrecan.122 |
Subchondral bone | Osteoblast cells | Ultracentrifugation | 30–150 nm.135 | – | – | – |
Infrapatellar fat pad | Infrapatellar fat pad MSCs | Ultrafiltration, precipitation and affinity-based capture | 30–150 nm | Articular chondrocyte | Chondroprotective effects and ameliorates gait abnormalities. | MiR100-5p-mediated inhibition of mTOR pathway.146 |
Tendon | Tendon stem cells | Ultracentrifugation | 40–200 nm | Tendon stem cells | Promote healing of injured tendon through regulating the metabolism of the tendon extracellular matrix and increases the ultimate stress and maximum loading in tendon. | Decrease MMP‐3 expression, increase TIMP‐3 and Col1a1 expression.150 |
Tendon | Tenocyte | Ultracentrifugation | – | Mesenchymal stem cells | Promote MSCs to undergo the tenogenic differentiation. | TGF-β-dependent manner.131 |
Ligament | Periodontal ligament fibroblasts | Ultracentrifugation and precipitation | 70–100 nm | MG-63 osteoblasts | Induce inflammation and inhibit osteogenic activity in osteoblasts | Upregulate the levels of IL-6 and TNF-α, inhibit OPG expression.157 |
Ligament | Periodontal ligament stem cells | Ultracentrifugation and affinity-based capture | 119 ± 12.1 nm155 | – | – | – |
Ligament | Periodontal ligament cells | Precipitation | 30–100 nm | Macrophage | Regulate macrophages function and maintain inflammation homeostasis. | Suppress IL-1β production via inhibiting NF-κB signaling pathway.156 |
