摘要
骨质疏松症已成为一个世界性的健康难题。作为一种强有力的干预措施,机械张力影响是骨再造的重要因素。然而,其背后的机制尚不明确。本文旨在研究机械性刺激诱导去卵巢大鼠骨髓间充质干细胞(OVX BMSCs)的成骨分化的可能机理。结果表明,机械张力 (IMS) 通过激活Runt相关转录因子2而促进OVX BMSCs的成骨分化。当细胞内调节的激酶1/2促分裂原活化蛋白激酶信号途径被阻断后,IMS对的成骨作用的影响减弱,当p38-MAPK信号通路的阻断对成骨作用的影响很小。此外,IMS对JNK的磷酸化水平没有影响。通过研究表明,机械张力通过 ERK1/2和 JNK-MAPK而不是p38 信号途径而促进去卵巢大鼠骨髓间充质干细胞的成骨作用。该发现可以应用于对骨质疏松症的物理治疗。
关键词: 骨髓间充质干细胞,间歇机械张力,MAPKs,成骨作用,骨质疏松,Runx2。
Current Molecular Medicine
Title:Mechanical Strain Promotes Osteogenesis of BMSCs from Ovariectomized Rats via the ERK1/2 but not p38 or JNK-MAPK Signaling Pathways.
Volume: 15 Issue: 8
关键词: 骨髓间充质干细胞,间歇机械张力,MAPKs,成骨作用,骨质疏松,Runx2。
摘要: Osteoporosis has become a world-wide health problem. As a promising intervention, mechanical strain is considered to be an important factor in bone remodeling. However, the underlying mechanisms are still not clarified clearly. In the present study, we aim to investigate the possible mechanism by which mechanical stimulation induces osteogenic differentiation of bone mesenchymal stem cells (BMSCs) from ovariectomized rats (OVX BMSCs). The results demonstrated that intermittent mechanical strain (IMS) promoted osteogenic differentiation of OVX BMSCs by activating Runt-related transcription factor 2 (Runx2). When the extracellular regulated kinase1/2-mitogen activated protein kinases (ERK1/2-MAPK) signaling pathway was blocked, the osteogenenic effects of IMS were diminished; while blocking of the p38-MAPK signaling pathway had little effect on subsequent osteogenic events. In addition, the phosphorylation level of JNK was not affected by IMS. Our results indicated that strain-induced osteogenic differentiation of OVX BMSCs may take effect via ERK1/2-MAPK not p38 or c-Jun N-terminal (JNK)-MAPK signaling pathway. These findings may have implications for physical treatment of osteoporosis in vitro.
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Mechanical Strain Promotes Osteogenesis of BMSCs from Ovariectomized Rats via the ERK1/2 but not p38 or JNK-MAPK Signaling Pathways., Current Molecular Medicine 2015; 15 (8) . https://dx.doi.org/10.2174/1566524015666150824143830
DOI https://dx.doi.org/10.2174/1566524015666150824143830 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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