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YK11 promotes osteogenic differentiation of BMSCs and repair of bone defects
Abstract:
The selective androgen receptor (AR) modulator YK11 promotes the anabolism of muscle cells and osteoblastic precursor cells. However, its effects on bone marrow-derived mesenchymal stem cells (BMSCs) and the repair of cranial bone defects are unknown. Here, the effects of different concentrations of YK11 on the osteogenic differentiation of BMSCs were determined. Subsequently, the AR was inhibited to investigate whether the effect of YK11 on the osteogenic differentiation of BMSCs was affected. A model of cranial defects was constructed to investigate the effects of the YK11-equipped hydrogel on cranial defect repair as well as the effects of YK11 on cranial defect repair after inhibiting the AR. Finally, the possible pathway of YK11 regulating the osteogenic differentiation of BMSCs was explored. Our results show 2 μM YK11 promoted the proliferation of BMSCs. A dose of 0.25-4 μM YK11 could promote osteogenesis of BMSCs, and the promoting effect was gradually enhanced with increasing concentration. In vivo, 0.5 and 1 mg/mL YK11 could promote the repair of cranial bone defects. After inhibiting the AR, the effects of YK11 on promoting both the osteogenic differentiation of BMSCs and repair of cranial defects were suppressed. YK11 may regulate the osteogenic differentiation of BMSCs through the BMP2 (bone morphogenetic protein 2)/Smad signaling pathway. In conclusion, YK11 promoted the osteogenic differentiation of BMSCs by activation on the AR. Meanwhile, YK11 promoted the repair of cranial bone defects in rats in vivo. The BMP2/Smad signaling pathway may be involved in the regulation of the osteogenic differentiation of BMSCs by YK11.
Insights
Selective androgen receptor modulator YK11 enhances bone marrow stem cell osteogenesis and cranial defect repair. Its effects are mediated through androgen receptor activation and potentially the BMP2/Smad pathway.
Area of Science:
- Biomedical Engineering
- Stem Cell Biology
- Regenerative Medicine
Background:
- Selective androgen receptor (AR) modulators like YK11 are known to promote muscle and bone precursor cell anabolism.
- The specific effects of YK11 on bone marrow-derived mesenchymal stem cells (BMSCs) and cranial bone defect repair remain uninvestigated.
Purpose of the Study:
- To determine the impact of YK11 on BMSC osteogenic differentiation and cranial bone defect repair.
- To elucidate the role of the AR in YK11's effects.
- To explore the signaling pathway involved in YK11-mediated osteogenesis.
Main Methods:
- Assessing YK11 concentrations on BMSC proliferation and osteogenic differentiation in vitro.
- Utilizing AR inhibition to confirm the mechanism of action.
- Employing a rat cranial defect model to evaluate YK11-loaded hydrogel efficacy in vivo.
- Investigating the BMP2/Smad signaling pathway.
Main Results:
- YK11 (2 μM) promoted BMSC proliferation; concentrations from 0.25-4 μM enhanced osteogenesis in a dose-dependent manner.
- YK11 (0.5 and 1 mg/mL) significantly promoted cranial bone defect repair in vivo.
- AR inhibition attenuated YK11's positive effects on both BMSC osteogenesis and cranial defect repair.
- Evidence suggests YK11 regulates BMSC osteogenic differentiation via the BMP2/Smad pathway.
Conclusions:
- YK11 promotes BMSC osteogenic differentiation through AR activation.
- YK11 facilitates cranial bone defect repair in a rat model.
- The BMP2/Smad signaling pathway is implicated in YK11's osteogenic regulation of BMSCs.
