Abstract

Bone marrow-derived mesenchymal stem cells (BMSCs) are widely used in tissue engineering for regenerative medicine due to their multipotent differentiation potential. However, their poor migration ability limits repair effects. Icariin (ICA), a major component of the Chinese medical herb Herba Epimedii, has been reported to accelerate the proliferation, osteogenic, and chondrogenic differentiation of BMSCs. However, it remains unknown whether ICA can enhance BMSC migration, and the possible underlying mechanisms need to be elucidated. In this study, we found that ICA significantly increased the migration capacity of BMSCs, with an optimal concentration of 1 μmol/L. Moreover, we found that ICA stimulated actin stress fiber formation in BMSCs. Our work revealed that activation of the MAPK signaling pathway was required for ICA-induced migration and actin stress fiber formation. In vivo, ICA promoted the recruitment of BMSCs to the cartilage defect region. Taken together, these results show that ICA promotes BMSC migration in vivo and in vitro by inducing actin stress fiber formation via the MAPK signaling pathway. Thus, combined administration of ICA with BMSCs has great potential in cartilage defect therapy.

Highlights

  • Osteoarthritis (OA), known as degenerative arthritis or joint disease, may lead to the loss of cartilage [1, 2]

  • bone marrow-derived mesenchymal stem cells (BMSCs) were obtained from rabbits, and their multipotent differentiation ability was detected by osteoplastic and chondrogenic differentiation

  • BMSCs developed into osteoblasts and chondrocytes after incubation with differentiation solution for 14 days

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Summary

Introduction

Osteoarthritis (OA), known as degenerative arthritis or joint disease, may lead to the loss of cartilage [1, 2]. BMSCs are easy to obtain, have abundant sources, and exhibit strong reproductive activity. BMSCs can be directed to differentiate into many types of cells damaged by disease under certain conditions. BMSCs can secrete active components that promote wound healing [5, 6]. BMSCs must successfully migrate to the wound to participate in repair processes. The low recruitment of BMSCs to target tissue deters their repair effect [7, 8]. Based on all these characteristics, enhancing the migration ability of BMSCs may be a promising research direction for treating cartilage defects

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