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To investigate the impact of secreted factors of rat bone marrow mesenchymal stem cells (MSCs) on the proliferation and migration of tenocytes and provide evidence for the development of MSC-based therapeutic methods of tendon injury. Rat bone marrow mesenchymal stem cell-derived conditioned medium (MSC-CM) promoted the proliferation of tenocytes within 24 h and decreased the percentage of tenocytes in G1 phase. MSC-CM activated the extracellular signal-regulated kinase1/2 (ERK1/2) signal molecules, while the ERK1/2 inhibitor PD98059 abrogated the MSC-CM-induced proliferation of tenocytes, decreased the fraction of tenocytes in the G1 phase and elevated p-ERK1/2 expression. Furthermore, MSC-CM promoted the migration of tenocytes within 6 h, enhanced the formation of filamentous actin (F-actin) and increased the cellular and nuclear stiffness of tenocytes. MSC-CM promotes tenocyte proliferation by changing cell cycle distribution via the ERK1/2 signaling pathway. MSC-CM-induced tenocyte migration was accompanied by cytoskeletal polymerization and increases in cellular and nuclear stiffness.

Interactions between tumors and mesenchymal stem cells (MSCs) can regulate cancer cell behavior and cancer progression. Rat bone marrow-derived MSCs (rMSCs) were isolated and purified by Percoll density gradient centrifugation. Conditioned media from rMSCs (MSC-CM) was prepared, and its role in cancer cell migration and the underlying molecular mechanism were investigated. MSC-CM increased the migration and up-regulated the expression of CXC chemokine receptor 4 (CXCR4) in rat hepatoma cells (CBRH-7919). F-actin remodeling was observed, and the Young's modulus was decreased in CBRH-7919 cells. A CXCR4 inhibitor suppressed the MSC-CM-induced CXCR4 expression and migration, restored the decrease in the Young's modulus and disrupted the formation of F-actin. MSC-CM thus promotes CBRH-7919 cell migration by lessening cell stiffness and increasing F-actin formation through up-regulation of CXCR4 expression. MSC-CM may therefore have a positive impact on cancer metastases and underlines a potential safety issue associated with clinical applications of MSCs.

To determine the possible beneficial effects of a synthetic mechano-growth factor E peptide (MGF-C25E) on the healing of rat Achilles tendon.A significantly increased Achilles functional index was found in the MGF-C25E-treated tendons relative to the saline-treated tendons. Macroscopic observation showed that the repair of MGF-C25E-treated (1000 ng/ml) tendons was superior to that of the saline-treated tendons. The mean value of the stiffness of the repaired tendons was significantly increased in the MGF-C25E-treated (1000 ng/ml) tendons relative to the saline-treated tendons. Moreover, histological analysis provided evidence of tissue remodeling and cell alignment.MGF-C25E plays an important role in promoting healing of injured rat tendon and could be used as a potential therapeutic factor for tendon repair.