Abstract
Transplantation of mesenchymal stem cells (MSCs) into osteoarthritis (OA) and rheumatoid arthritis (RA) patients has been studied as a therapeutic tool for regeneration of damaged cartilage. MSCs have several beneficial effects, including immunomodulatory activity, and release various paracrine factors. Despite their abundant beneficial effects, transplantation of naive MSCs is hampered by heterogeneous populations of differentiated and undifferentiated stem cells. However, transplantation of differentiated MSCs overcomes the problem of transplantation of naive MSCs. Thus, to repair damaged tissue, a therapeutic strategy based on the use of differentiated MSCs is needed to treat RA or OA patients. Here, we summarize methods that can regulate differentiation of MSCs into chondrocytes by small molecules or miRNAs, and suggest the capacity of patient tissue-derived MSCs as a therapeutic strategy for treatment of OA or RA patients.
Highlights
Disruption of cartilage homeostasis is induced by combinations of biological mediators, which leads to the development of joint diseases such as osteoarthritis (OA) or rheumatoid arthritis (RA) [1, 2]
mesenchymal stem cells (MSCs) transplantation has been suggested as a therapeutic tool for treatment of joint diseases [7,8,9]
We focused on the role of MSCs as a therapeutic strategy for treatment of OA or RA patients, as well as the methods required to induce differentiation into chondrogenic cells by miRNAs and small molecules
Summary
Disruption of cartilage homeostasis is induced by combinations of biological mediators, which leads to the development of joint diseases such as osteoarthritis (OA) or rheumatoid arthritis (RA) [1, 2]. MSCs transplantation has been suggested as a therapeutic tool for treatment of joint diseases [7,8,9]. MicroRNAs (miRNAs) can induce differentiation of MSCs into various cell types, including myoblasts, neurons, adipocytes, osteoblasts, and chondrocytes [17]. It has been suggested that MSCs that have been differentiated into specific cell types by tissue-specific miRNAs be transplanted into patients for the treatment of joint disease. We focused on the role of MSCs as a therapeutic strategy for treatment of OA or RA patients, as well as the methods required to induce differentiation into chondrogenic cells by miRNAs and small molecules. We discuss the possibility for use of miRNAs or small molecules as a tool for differentiation of MSCs into chondrogenic cells
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