OBJECTIVE: In this study, we aim to explore the roles and potential mechanisms of hADSCs in cutaneous wound healing.
METHODS: hADSCs were obtained from human subcutaneous fat. Adipocytes and osteocytes differentiated from hADSCs were determined by staining with Oil Red O and alkaline phosphatase (ALP), respectively. We assessed the effects of hADSCs and hADSC conditional medium (CM) on wound healing in an injury model of mice. Then, we investigated the biological effects of hADSCs on human keratinocytes HaCAT cells in vitro.
RESULTS: The results showed that hADSCs could be successfully differentiated into osteogenic and lipogenic cells. hADSCs and hADSCs-CM significantly promote skin wound healing in vivo. hADSCs significantly promoted HaCAT cell proliferation and migration by activating the Notch signaling pathway and activated the AKT signaling pathway by Rps6kb1 kinase in HaCAT cells. In addition, we found that hADSCs-mediated activation of Rps6kb1/AKT signaling was dependent on the Notch signaling pathway.
CONCLUSIONS: We demonstrated that hADSCs can promote skin cell-HaCAT cell proliferation and migration via the Notch pathway, suggesting that hADSCs may provide an alternative therapeutic approach for the treatment of skin injury.
目的:在本研究中,我们旨在探讨hADSC在皮肤伤口愈合中的作用和潜在机制。
方法:hADSC从人皮下脂肪获得。通过油红O和碱性磷酸酶(ALP)染色确定从hADSCs分化的脂肪细胞和骨细胞,分别。我们在小鼠损伤模型中评估了hADSC和hADSC条件培养基(CM)对伤口愈合的影响。然后,我们在体外研究了hADSCs对人角质形成细胞HaCAT细胞的生物学效应。
结果:结果显示hADSCs可以成功分化为成骨和成脂细胞。hADSC和hADSC-CM在体内显著促进皮肤创伤愈合。hADSCs通过激活Notch信号通路和Rps6kb1激酶激活AKT信号通路显著促进HaCAT细胞增殖和迁移。此外,我们发现hADSC介导的Rps6kb1/AKT信号激活依赖于Notch信号通路。
结论:我们证明hADSCs可以通过Notch途径促进皮肤细胞-HaCAT细胞的增殖和迁移,提示hADSC可能为皮肤损伤的治疗提供替代治疗方法。