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首页> 外文期刊>Journal of Cellular Physiology >Bradykinin Regulates Osteoblast Differentiation by Akt/ERK/NFκB Signaling Axis
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Bradykinin Regulates Osteoblast Differentiation by Akt/ERK/NFκB Signaling Axis

机译:缓激肽调节成骨细胞分化一种蛋白激酶ERK / NFκB信号轴

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摘要

Bradykinin (BK), a well known mediator of pain and inflammation, is also known to be involved in the process of bone resorption. The present study therefore evaluated the role of BK in osteoblast lineage commitment. Our data showed that BK inhibits the migration of bone marrow mesenchymal stem cells, but does not affect their viability. Moreover, BK also inhibits osteoblastic differentiation by significantly downregulating the levels of mRNAs for osteopontin, runX2, col24, osterix, osteocalcin genes and bone mineralization (P<0.05). Further, BK was found to elicit the BK receptors (BDKR1 and BDKR2) mediated activation of ERK1/2 and Akt pathways, which finally led to the activation of NFκB. BK also promoted the osteoclast differentiation of bone marrow derived preosteoclast cells by upregulating the expression of c-fos, NFATC1, TRAP, clcn7, cathK, and OSCAR genes and increasing TRAP activity through NFκB pathway. In conclusion, our data suggest that BK decreases the differentiation of osteoblasts with concomitant increase in osteoclast formation and thus provides new insight into the mechanism of action of BK in modulating bone resorption. J. Cell. Physiol. 229: 2088-2105, 2014.
机译:缓激肽(BK),一个众所周知的疼痛和中介炎症,也参与了骨吸收的过程。因此评估BK在成骨细胞的作用血统的承诺。抑制骨髓间叶细胞的迁移干细胞,但并不影响他们的生存能力。此外,汉堡王也抑制成骨细胞的分化通过显著下调runX2的骨桥蛋白mrna水平,col24 osterix,骨钙素基因和骨头矿化(P < 0.05)。引起BK受体(BDKR1和BDKR2)调节ERK1/2和Akt通路的激活,最终导致NFκB的激活。也促进了破骨细胞分化骨髓衍生preosteoclast细胞NFATC1上调c-fos的表达,陷阱,clcn7 cathK,奥斯卡基因和增加陷阱活动通过NFκB通路。结论:我们的数据表明,BK减少成骨细胞的分化破骨细胞形成和伴随的增加这样的机制提供了新的见解BK在调节骨吸收的作用。细胞。

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