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首页> 外文期刊>Journal of Biomechanics >Cyclic strain enhances matrix mineralization by adult human mesenchymal stem cells via the extracellular signal-regulated kinase (ERK1/2) signaling pathway.
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Cyclic strain enhances matrix mineralization by adult human mesenchymal stem cells via the extracellular signal-regulated kinase (ERK1/2) signaling pathway.

机译：循环应变可通过细胞外信号调节激酶（ERK1 / 2）信号传导途径增强成人间充质干细胞的基质矿化作用。

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摘要

Physical stimuli play critical roles in the development, regeneration, and pathology of many mesenchymal tissues, most notably bone. While mature bone cells, such as osteoblasts and osteocytes, are clearly involved in these processes, the role of their progenitors in mechanically mediated tissue responses is unknown. In this study, we investigated the effect of cyclic substrate deformation on the proliferation and osteogenic differentiation of human mesenchymal stem cells (hMSCs). Application of equibiaxial cyclic strain (3%, 0.25Hz) to hMSCs cultured in osteogenic media inhibited proliferation and stimulated a 2.3-fold increase in matrix mineralization over unstrained cells. The strain stimulus activated the extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein kinase pathways, but had no effect on c-Jun N-terminal kinase phosphorylation or activity. Strain-induced mineralization was largely mediated by ERK1/2 signaling, as inhibition of ERK1/2 attenuated calcium deposition by 55%. Inhibition of the p38 pathway resulted in a more mature osteogenic phenotype, suggesting an inhibitory role for p38 signaling in the modulation of strain-induced osteogenic differentiation. These results demonstrate that mechanical signals regulate hMSC function, suggesting a critical role for physical stimulation of this specific cell population in mesenchymal tissue formation.
机译：物理刺激在许多间充质组织（尤其是骨骼）的发育，再生和病理中起关键作用。尽管成熟的骨细胞（例如成骨细胞和骨细胞）显然参与了这些过程，但其祖细胞在机械介导的组织反应中的作用尚不清楚。在这项研究中，我们调查了循环基质变形对人间充质干细胞（hMSCs）增殖和成骨分化的影响。向在成骨培养基中培养的hMSC应用等双轴循环应变（3％，0.25Hz）可以抑制增殖，并比未应变的细胞刺激基质矿化增加2.3倍。菌株刺激激活了细胞外信号调节激酶（ERK1 / 2）和p38丝裂原激活的蛋白激酶途径，但对c-Jun N端激酶的磷酸化或活性没有影响。应变诱导的矿化作用很大程度上由ERK1 / 2信号传导介导，因为对ERK1 / 2的抑制作用使钙沉积减少了55％。 p38途径的抑制导致更成熟的成骨表型，表明在调节菌株诱导的成骨分化中p38信号的抑制作用。这些结果表明机械信号调节hMSC功能，暗示物理刺激该特定细胞群体在间充质组织形成中的关键作用。

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