Current stem cell research & therapy · 2026
Wnt5a-Modified Mesenchymal Stem Cells Promote the Repair of Cartilage Defects.
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Wu Zhifang, Zheng Fosheng, Luo Yiwen, Xu Liangliang, Gao Zhao
Аннотация
INTRODUCTION/OBJECTIVE: Cartilage tissue exhibits limited ability to self-renew after injury, which leads to mobility impairment and even disability. To investigate the regulatory effect of Wnt5a on chondrogenesis of Mesenchymal Stem Cells (MSCs), and evaluate the application effect of Wnt5a-overexpressing MSCs in cartilage defect repair.
METHODS: Transwell assay and scratch assay were used to check cell migration capacity, and chondrogenic induction assay was employed to verify the level of chondrogenic differentiation potential. Western Blot was performed to detect the relative levels of protein. An animal model of cartilage defect was established, and Wnt5a-overexpressing MSCs were implanted to assess the repair effect.
RESULTS: Compared with the empty vector control, Wnt5a overexpression significantly enhanced the proliferation activity and migration ability of MSCs, and enhanced the chondrogenic potential of MSCs. Moreover, Wnt5a overexpression could significantly up-regulate the protein expression levels of p-Akt and p-JNK in MSCs, thereby activating the PI3K/AKT and JNK signaling pathways. Finally, the in vivo experiments confirmed that MSCs overexpressing Wnt5a could effectively promote the repair of cartilage defects.
DISCUSSION: Modifying MSCs with Wnt5a to enhance their biological functions can be used to improve cartilage defect repair.
CONCLUSION: Wnt5a controls MSC proliferation, migration, and chondrogenesis, likely through the PI3K/AKT and JNK signaling pathways. Wnt5a-overexpressing MSCs have the effect of promoting cartilage defect repair.
METHODS: Transwell assay and scratch assay were used to check cell migration capacity, and chondrogenic induction assay was employed to verify the level of chondrogenic differentiation potential. Western Blot was performed to detect the relative levels of protein. An animal model of cartilage defect was established, and Wnt5a-overexpressing MSCs were implanted to assess the repair effect.
RESULTS: Compared with the empty vector control, Wnt5a overexpression significantly enhanced the proliferation activity and migration ability of MSCs, and enhanced the chondrogenic potential of MSCs. Moreover, Wnt5a overexpression could significantly up-regulate the protein expression levels of p-Akt and p-JNK in MSCs, thereby activating the PI3K/AKT and JNK signaling pathways. Finally, the in vivo experiments confirmed that MSCs overexpressing Wnt5a could effectively promote the repair of cartilage defects.
DISCUSSION: Modifying MSCs with Wnt5a to enhance their biological functions can be used to improve cartilage defect repair.
CONCLUSION: Wnt5a controls MSC proliferation, migration, and chondrogenesis, likely through the PI3K/AKT and JNK signaling pathways. Wnt5a-overexpressing MSCs have the effect of promoting cartilage defect repair.