Table 1.
Exosome Origin Cell Source | Study Design | Animal Models | miRNA | Result(s) | Target(s) | Reference |
---|---|---|---|---|---|---|
Human BMSCs | in vitro | - | miR-320c | Upregulates SOX9 and downregulates MMP13 expression in OA chondrocyte. | Not mentioned | [78] |
Human BMSCs | in vitro | - | miR-95-5p | Enhances histone H3 acetylation and maintains the function of articular chondrocytes. Promotes SOX9, COL2A1 and Aggrecan expression and enhances cartilage development. | HDAC2/8 | [79] |
Human chondrocytes | in vitro | - | miR-8485 | Activates Wnt/β-catenin pathways. Promotes chondrogenic differentiation of hBMSCs. | GSK3B, DACT1 | [80] |
Human BMSCs | in vitro and in vivo |
Mice | miR-92a-3p | Promotes cartilage proliferation. In both MSCs and PHCs, promotes matrix genes expression and inhibits WNT5A expression. | WNT5A | [81] |
Human BMSCs | in vitro and in vivo |
Rats | miR-26a-5p | It was shown that the damage of synovial fibroblasts is suppressed in vitro, and the OA damage is alleviated in vivo. | PTGS2 | [82] |
Human IPFP MSCs | in vitro and in vivo |
Mice | miR-100-5p | Protects cartilage from damage and ameliorate gait patterns of DMM-induced OA mice. | mTOR | [83] |
Human SMSCs | in vitro and in vivo |
Rats | miR-140-5p | Enhances the proliferation and migration of ACs, and the progression of early OA and prevents severe damage to knee articular cartilage in the OA rats. | RalA | [84] |
hBMSC: human bone marrow-derived MSC, IPFP: infrapatellar fat pad, SMSC: synovium-derived MSC, MSC: mesenchymal stem cell, PHC: primary human chondrocytes, WNT5A: Wnt family member 5A, OA: osteoarthritis, SOX9: SRY-box transcription factor 9, MMP13: matrix metalloproteinase 13, COL2A1: Collagen type II alpha 1, DMM: destabilization of the medial meniscus, AC: articular cartilage, PTGS2: Prostaglandin-endoperoxide synthase 2, HDAC: histone deacetylase, mTOR: mammalian target of rapamycin, RalA: Ras-related protein, GSK-3β: glycogen synthase kinase 3 beta, DACT1: dishevelled binding antagonist of beta catenin 1.