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首页> 外文期刊>Journal of Biomechanics >Mechanical stimulation and mitogen-activated protein kinase signaling independently regulate osteogenic differentiation and mineralization by calcifying vascular cells
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Mechanical stimulation and mitogen-activated protein kinase signaling independently regulate osteogenic differentiation and mineralization by calcifying vascular cells

机译：机械刺激和丝裂原激活的蛋白激酶信号传导通过钙化血管细胞独立调节成骨分化和矿化

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摘要

Ectopic calcification of vascular tissue is associated with several cardiovascular pathologies and likely involves active regulation by vascular smooth muscle cells and osteoblast-like vascular cells. This process often occurs in sites with altered mechanical environments, suggesting a role for mechanical stimuli in calcification. In this study, we investigated the effect of mechanical stimulation on the proliferation, osteogenic differentiation, calcification, and mitogen-activated protein kinase (MAPK) signaling in calcifying vascular cells (CVCs), a subpopulation of aortic smooth muscle cells putatively involved in vascular calcification. Application of equibiaxial cyclic strain (7%, 0.25 Hz) to CVCs had no effect on cell proliferation, but accelerated alkaline phosphatase expression and significantly increased mineralization by 3.1-fold over unstrained cells. Fluid motion in the absence of strain also enhanced mineralization, but to a lesser degree. Because MAPK pathways mediate mechanically regulated osteoblast differentiation, we tested whether similar signaling was involved in mineralization by CVCs. In static cultures, pharmacological inhibition of the extracellular sign at-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase pathways significantly attenuated mineral production by as much as -94%, compared with uninhibited CVCs. Strikingly, although mechanical stimulation activated each of the MAPK pathways, inhibition of these pathways had no effect on the mechanically induced enhancement of alkaline phosphatase activity or mineralization. These novel data indicate that mechanical signals regulate calcification by CVCs, and although MAPK signaling is critical to CVC osteogenic differentiation and mineralization, it is not involved directly in transduction of mechanical signals to regulate these processes under the conditions utilized in this study. (C) 2004 Elsevier Ltd. All rights reserved.
机译：血管组织的异位钙化与几种心血管疾病有关，并且可能涉及血管平滑肌细胞和成骨样血管细胞的主动调节。该过程通常发生在机械环境改变的部位，提示机械刺激在钙化中的作用。在这项研究中，我们调查了机械刺激对钙化血管细胞（CVC）（假定参与血管钙化的主动脉平滑肌细胞亚群）中增殖，成骨分化，钙化和丝裂原活化蛋白激酶（MAPK）信号传导的影响。将等双轴循环应变（7％，0.25 Hz）应用于CVC对细胞增殖没有影响，但是加速了碱性磷酸酶的表达，并使矿化作用比未应变的细胞明显增加了3.1倍。在没有应变的情况下的流体运动也增强了矿化作用，但是程度较小。由于MAPK途径介导机械调节的成骨细胞分化，因此我们测试了CVC的矿化是否涉及相似的信号传导。在静态培养物中，与未抑制的CVC相比，药理学抑制细胞外信号调节激酶（ERK1 / 2），p38 MAPK和c-Jun N端激酶途径可显着降低矿物质产生-94％。令人惊讶的是，尽管机械刺激激活了每个MAPK途径，但抑制这些途径对机械诱导的碱性磷酸酶活性增强或矿化没有影响。这些新颖的数据表明，机械信号调节CVC的钙化，尽管MAPK信号对于CVC成骨细胞的分化和矿化至关重要，但在本研究中使用的条件下，它不直接参与机械信号的传导以调节这些过程。 （C）2004 Elsevier Ltd.保留所有权利。

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