4.5 Article

Vaspin promotes chondrogenic differentiation of BMSCs via Akt activation in osteoarthritis

Journal

BMC MUSCULOSKELETAL DISORDERS
Volume 23, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12891-022-05295-9

Keywords

Vaspin; Bone mesenchymal stem cells; Chondrocyte; Akt

Funding

  1. National Natural Science Foundation of China [81802233]
  2. Peking University International Hospital Research Grant [YN2018QN02]

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This study investigates the role of Vaspin on the chondrogenic differentiation of BMSCs and chondrocytes survival, and its involvement of Akt activation. Vaspin promotes the chondrogenic differentiation of BMSCs and chondrocyte survival by activating the Akt pathway. It also increases the expression of markers in cartilage formation and extracellular matrix secretion. These findings provide new insights into the potential ability of Vaspin to ameliorate the chondrogenic differentiation of BMSCs and chondrocyte survival in osteoarthritis (OA).
Background The aim of this study was to investigate the role of Vaspin on the chondrogenic differentiation of bone mesenchymal stem cells (BMSCs), and its effect on chondrocyte survival and ECM secretion. We also assessed whether the Akt activation participates in these processes. Methods In vivo, immunohistochemistry was used to examine the positive rate of the protein expressions of Akt in Wistar rat articular cartilage and subchondral bone after Vaspin intraperitoneal injection for 14 days. In vitro, we isolated and expanded BMSCs from Wistar rats, and further cultured BMSCs as pellets in a chondrogenic-differentiation medium supplemented with different concentrations of Vaspin. After 21 days, the pellets were processed for cell counting kit assay. The mRNA level of Akt, SOX9 and COL2A1 in the pellets were investigated using quantitative Real-Time polymerase chain reaction, and the protein level of COMP was detected using western blot. Results During the chondrogenic differentiation of BMSCs, Vaspin promoted the chondrogenic differentiation of BMSCs and chondrocyte survival by activating the Akt pathway. These effects were significantly reduced by treatment with an Akt inhibitor. Moreover, Vaspin promoted chondrogenic differentiation of BMSCs by increasing the expression of markers in cartilage formation and extracellular matrix secretion. Furthermore, our study also found that Vaspin could increase Akt expression in cartilage cavities and subchondral bone in vivo. Conclusion These findings demonstrate that Vaspin can promote the chondrogenic differentiation of BMSCs and chondrocyte survival via Akt activation. Our study provides new insights into the potential ability of Vaspin to ameliorate the chondrogenic differentiation of BMSCs and chondrocyte survival in OA.

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