Static Magnetic Field Promotes Proliferation, Migration, Differentiation, and AKT Activation of Periodontal Ligament Stem Cells

被引:12
|
作者
Zhang, Kun [1 ]
Ge, WenBin [1 ]
Luo, ShiTong [1 ]
Zhou, Zhi [2 ]
Liu, YaLi [1 ]
机构
[1] Kunming Med Univ, Sch & Hosp Stomatol, Kunming, Peoples R China
[2] Yunnan Univ, Dept Orthodont, Affiliated Hosp, Kunming, Peoples R China
基金
中国国家自然科学基金;
关键词
Static magnetic fields; Proliferation; Migration; Osteogenic differentiation; Protein kinase B; OSTEOGENIC DIFFERENTIATION; VIABILITY; STIMULATION; IMPLANTS; PI3K/AKT;
D O I
10.1159/000524291
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Periodontal ligament stem cells (PDLSCs) possess self-renewal and multilineage differentiation potential and exhibit great potential for the treatment of bone tissue defects caused by inflammation. Previous studies have indicated that static magnetic field (SMF) can enhance the proliferation and differentiation of mesenchymal stem cells (MSCs). SMF has been widely used to repair bone defects and for orthodontic and implantation treatment. In this study, we revealed that a 320 mT SMF upregulates the protein expression levels of cytokines such as MCM7 and PCNA in proliferating PDLSCs. Cell counting kit-8 results revealed that the SMF group had higher optical density values than the control group. The ratio of cells in the S phase to those in the G2/M phase was significantly increased after exposure to a 320 mT SMF. In scratch assays, the SMF-treated PDLSCs exhibited a higher migration rate than the sham-exposed group after 24 h of culture, indicating that the SMF promoted the migratory ability of PDLSCs. The activity level of the early differentiation marker alkaline phosphatase and the late marker matrix mineralization, as well as osteoblast-specific gene and protein expression, were enhanced in PDLSCs exposed to the SMF. Furthermore, AKT signaling pathway was activated by SMF. Our data demonstrated that the potential mechanism of action of SMF may enhance PDLSCs proliferation and osteogenic differentiation by activating the phosphorylated AKT pathway. The elucidation of this molecular mechanism may lead to a better understanding of bone repair responses and aid in improved stem cell-mediated regeneration.
引用
收藏
页码:317 / 326
页数:10
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