Liu Silin, Jin Zuolin, Cao Meng, Hao Dandan, Li Chunrong, Li Doudou, Zhou Weiwei
The Fourth Military Medical University, School of Stomatology, Department of Orthodontics, State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi Clinical Research Center for Oral Diseases, Xi'an, China.
Affiliated Hospital of Chifeng University, Department of Orthodontics, Inner Mongolia, China.
Genet Mol Biol. 2021 Sep 29;44(3):e20200461. doi: 10.1590/1678-4685-GMB-2020-0461. eCollection 2021.
Osteoporosis is a condition of the skeleton that mainly results from estrogen deficiency. Periostin is a matricellular component in bone that is involved in osteoblast differentiation. However, how Periostin promotes osteogenesis remains largely unknown. Here, we isolated bone marrow skeletal stem cells (BMSCs) derived from an ovariectomy (OVX)-induced osteoporosis rat model and the effects of periostin on BMSCs derived from OVX rats (OVX-BMSCs) were assessed. Overexpression of periostin enhanced alkaline phosphatase (ALP) and alizarin red staining in OVX-BMSCs as well as the osteogenic genes OCN, BSP and Runx2. ILK is a downstream effector of signals from the extracellular matrix and participates in bone homeostasis. Overexpression of periostin also increased expression of protein levels for ILK, as well as the downstream targets pAkt and pGSK3β. Suppression of ILK or Akt partially suppressed the enhancement of osteogenic ability induced by periostin overexpression in OVX-BMSCs. Thus, periostin may promote the osteogenic ability of OVX-BMSCs through actions on the ILK/Akt/GSK3β axis.
骨质疏松症是一种主要由雌激素缺乏引起的骨骼疾病。骨膜蛋白是骨骼中的一种基质细胞成分,参与成骨细胞分化。然而,骨膜蛋白如何促进骨生成在很大程度上仍不清楚。在此,我们分离了来自卵巢切除(OVX)诱导的骨质疏松大鼠模型的骨髓骨骼干细胞(BMSC),并评估了骨膜蛋白对来自OVX大鼠的BMSC(OVX-BMSC)的影响。骨膜蛋白的过表达增强了OVX-BMSC中的碱性磷酸酶(ALP)和茜素红染色,以及成骨基因OCN、BSP和Runx2。整合素连接激酶(ILK)是细胞外基质信号的下游效应器,参与骨稳态。骨膜蛋白的过表达还增加了ILK蛋白水平的表达,以及下游靶点pAkt和pGSK3β。抑制ILK或Akt可部分抑制OVX-BMSC中骨膜蛋白过表达诱导的成骨能力增强。因此,骨膜蛋白可能通过作用于ILK/Akt/GSK3β轴来促进OVX-BMSC的成骨能力。