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首页> 外文期刊>Annals of Biomedical Engineering >Involvement of p38MAPK/NF-κB Signaling Pathways in Osteoblasts Differentiation in Response to Mechanical Stretch
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Involvement of p38MAPK/NF-κB Signaling Pathways in Osteoblasts Differentiation in Response to Mechanical Stretch

机译：p38MAPK /NF-κB信号通路参与成骨细胞分化对机械拉伸的响应

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摘要

Bone morphogenetic proteins (BMPs) are known to be important in osteoblasts’ response to mechanical stimuli. BMPs/Smad signaling pathway has been demonstrated to play a regulatory role in the mechanical signal transduction in osteoblasts. However, little is currently known about the Smad independent pathway in osteoblasts differentiation in mechanical loading. In this study, MC3T3-E1 cells were subjected to mechanical stretch of 2000 micro-stain (με) at 0.5 Hz, in order to investigate the involvement of p38MAPK and NF-κB signaling pathways in mechanical response in osteoblasts. We found BMP-2/BMP-4 were up-regulated by mechanical stretch via the earlier activation of p38MAPK and NF-κB signaling pathways, which enhanced osteogenic gene expressions including alkaline phosphatase (ALP), collagen type I (Col I) and osteocalcin (OCN), and the expressions of these osteogenic genes were remarkably decreased with Noggin (an inhibitor for BMPs signals) pretreatment. Furthermore, BMP-2/BMP-4 expressions were suppressed by PDTC, an inhibitor of NF-κB pathway and SB203580, an inhibitor of p38MAPK pathway, respectively, leading to the declined levels of ALP, Col I and OCN. Interestingly, blocking in p38MAPK pathway can also cause the inactivation of NF-κB pathway in mechanical stretch. Collectively, the results indicate during mechanical stretch p38MAPK and NF-κB signaling pathways are activated first, and then up-regulate BMP-2/BMP-4 to enhance osteogenic gene expressions. Moreover, p38MAPK and NF-κB signals have cross-talk in regulation of BMP-2/BMP-4 in mechanical response.
机译：众所周知，骨形态发生蛋白（BMP）对于成骨细胞对机械刺激的反应至关重要。已证明BMP / Smad信号通路在成骨细胞的机械信号转导中起调节作用。然而，目前关于机械负载中成骨细胞分化中的Smad独立途径了解甚少。在这项研究中，为了研究p38MAPK和NF-κB信号通路在成骨细胞的机械反应中的作用，对MC3T3-E1细胞进行了0.5 Hz的2000微污点（με）的机械拉伸。我们发现BMP-2 / BMP-4通过p38MAPK和NF-κB信号通路的早期激活而通过机械拉伸上调，从而增强了成骨基因表达，包括碱性磷酸酶（ALP），I型胶原（Col I）和骨钙蛋白（OCN），并且用Noggin（一种BMPs信号抑制剂）预处理显着降低了这些成骨基因的表达。此外，PDMP（NF-κB途径的抑制剂）和SB203580（p38MAPK途径的抑制剂）分别抑制了BMP-2 / BMP-4的表达，导致ALP，Col I和OCN的水平降低。有趣的是，p38MAPK途径的阻断也可导致机械牵张中NF-κB途径的失活。总体而言，该结果表明在机械拉伸过程中，p38MAPK和NF-κB信号通路首先被激活，然后上调BMP-2 / BMP-4以增强成骨基因表达。此外，p38MAPK和NF-κB信号在机械反应中对BMP-2 / BMP-4的调节中存在串扰。

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