Influence of Transmural Pressure and Cytoskeletal Structure on NF-κB Activation in Respiratory Epithelial Cells.
Influence of Transmural Pressure and Cytoskeletal Structure on NF-κB Activation in Respiratory Epithelial Cells.
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DOI：
10.1007/s12195-010-0138-7
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发表时间：
2010-12-01
影响因子：
2.8
通讯作者：
Ghadiali, Samir N.
中科院分区：
文献类型：
--
作者：
Huang, Yan;Haas, Caroline;Ghadiali, Samir N.
关键词：
呼吸道上皮细胞暴露于复杂的机械力，这些机械力通常在诸如中耳炎和急性肺损伤的病理状况期间被调节。将这些机械力转换为改变的炎症信号可能在疾病状况和炎症的持续性中起重要作用。在这项研究中，我们研究了静态和振荡压力如何改变NF-κB炎症通路的激活，以及肌动蛋白细胞骨架的变化如何影响压力到NF-κB激活的机械转导。一个在体外系统被用来施加静态和振荡的压力，肺泡上皮细胞培养在气液界面。用Latrunculin A和Jasplakinase改变细胞骨架和紧密连接结构，用ELISA监测NF-κB的活化。结果表明，静态和振荡压力都可以激活NF-κB，并且这种激活仅在低振荡频率下具有幅度依赖性。与未加载对照相比，Jasplakin处理的细胞在标准化NF-κB活化方面没有表现出显著变化，而Latrunculin处理的细胞仅在低频或静压下表现出标准化NF-κB活化的增加。这些结果表明，改变肌动蛋白细胞骨架可能是一种有用的方式，以减轻压力的机械转导到炎症信号。
Respiratory epithelial cells are exposed to complex mechanical forces which are often modulated during pathological conditions such as Otitis Media and acute lung injury. The transduction of these mechanical forces into altered inflammatory signaling may play an important role in the persistence of disease conditions and inflammation. In this study, we investigated how static and oscillatory pressures altered the activation of NF-κB inflammatory pathways and how changes in the actin cytoskeleton influenced the mechanotransduction of pressure into NF-κB activation. An in vitro system was used to apply static and oscillatory pressures to alveolar epithelial cells cultured at an air–liquid interface. Latrunculin A and Jasplakinolide were used to alter the cytoskeleton and tight-junction structure and ELISA was used to monitor activation of NF-κB. Results indicate that both static and oscillatory pressures can activate NF-κB and that this activation is magnitude-dependent at low oscillation frequencies only. Jasplakinolide treated cells did not exhibit significant changes in normalized NF-κB activation compared to unloaded controls while Latrunculin treated cells exhibited increases in normalized NF-κB activation only at low frequency or static pressures. These results indicate that altering the actin cytoskeleton may be a useful way to mitigate the mechanotransduction of pressure forces into inflammatory signaling.
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影响因子：
6.9
作者：
Jafari, B;Ouyang, B;Quinn, DA
通讯作者：
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影响因子：
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DOI：
10.1152/ajplung.00510.2005
发表时间：
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Ghadiali, S. N.
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