Nuclear factor of activated T cell mediates proinflammatory gene expression in response to mechanotransduction

被引:8
作者
Aydemir, Ayse B. Celil [1 ]
Lee, Stephenie [1 ]
Kim, Dae Won [2 ]
Gardner, Thomas R. [1 ]
Prince, Daniel [1 ]
Ahn, Jae Mok [3 ]
Lee, Francis Young-In [1 ]
机构
[1] Columbia Univ, Dept Orthopaed Surg, New York, NY 10032 USA
[2] Columbia Med Ctr, Dept Surg, New York, NY USA
[3] Hallym Univ, Chunchon, South Korea
来源
SKELETAL BIOLOGY AND MEDICINE, PT B: DISEASE MECHANISMS AND THERAPEUTIC CHALLENGES | 2007年 / 1117卷
关键词
NFAT; fluid shear stress; Cox2; FLUID-FLOW; SHEAR-STRESS; KINASE;
D O I
10.1196/annals.1402.004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Bone adapts to its environment. Osteoblasts and osteocytes are subject to mechanical load in vivo. It has been shown that osteoblasts alter cytokine expression in response to mechanical loading. However, signal transduction pathways that mediate bone cell response to mechanical stimuli have not been elucidated. In this study, we report an increase in proinflammatory gene expression in response to fluid shear stress (FSS) in human mesenchymal stem cells (hMSCs) and mouse preosteoblasts. Fluid shear stress (FSS)-induced effect was blocked by the inhibition of the calcineurin-NFATc1 axis, thus implicating a role for nuclear factor of activated T cells (NFAT) signaling in mechanotransduction.
引用
收藏
页码:138 / 142
页数:5
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