Bone marrow stromal cells enhance chondrocyte function and autophagy via mTOR signaling.

This study was focused on exploring the potential therapeutic utility of bone marrow stromal cells (BMSCs) as an approach to treating temporomandibular joint osteoarthritis (TMJOA), with a particular focus on their effects on the proliferation of condylar chondrocytes, the process of osteogenic differentiation, and the regulation of autophagic activity. After culturing BMSCs, their surface antigen expression profiles were evaluated, validating their identities based on high levels of CD54 and CD90 expression together with low levels of CD34 and CD45 expression. Alizarin Red and Oil Red O staining were respectively used to test the ability of these cells to differentiate into osteoblasts and adipocytes, respectively. When co-cultured with condylar chondrocytes, these BMSCs induced significantly enhanced proliferative activity and osteogenic differentiation. When autophagic activity was analyzed via qPCR and Western immunoblotting, BMSCs were found to promote condylar chondrocyte autophagy as demonstrated by increases in the expression of ATG5, Beclin-1, and LC3-II, together with reduced mTOR phosphorylation. The mTOR-specific inhibitor rapamycin and the agonist SPQ were used to confirm the importance of mTOR signaling in the process of BMSC-induced autophagic activity. Based on these results, BMSCs appear to offer a high degree of therapeutic utility in TMJOA through their ability to enhance the proliferative and autophagic activity of chondrocytes together with their osteogenic differentiation. Interventions that target the mTOR pathway may be of particular value for the treatment of TMJOA. Additional in vivo research will be essential to validate these in vitro results and to clarify the long-term joint health outcomes associated with BMSC therapy.