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流体剪切应力诱导培养的人内皮细胞中c-fos的合成及核定位。

Fluid shear stress induces synthesis and nuclear localization of c-fos in cultured human endothelial cells.

作者信息

Ranjan V, Diamond S L

机构信息

Department of Chemical Engineering, State University of New York, Buffalo 14260.

出版信息

Biochem Biophys Res Commun. 1993 Oct 15;196(1):79-84. doi: 10.1006/bbrc.1993.2218.

DOI:10.1006/bbrc.1993.2218
PMID:8216338
Abstract

Quiescent cultured primary human umbilical vein endothelial cells were exposed to low levels (4 dynes/cm2) or arterial levels (25 dynes/cm2) of steady laminar shear stress for one hour. Intracellular c-fos protein was measured by immunocytochemistry and quantitative fluorescence video microscopy. The nuclear-localized c-fos protein level was 5.4 +/- 2.0 fold higher (p < 0.01) in the cells exposed to arterial levels of shear stress as compared to the cells maintained in stationary culture. In contrast, the cells exposed to low levels of shear stress showed diffuse but slightly elevated levels of c-fos (2.4 +/- 0.73 times higher than control; p < 0.01) without preferential nuclear localization. The protein kinase C inhibitor, H7 (10 microM) significantly attenuated the induction of c-fos by 50% in cells exposed to arterial shear stress for 1 hour.

摘要

将静止培养的原代人脐静脉内皮细胞暴露于低水平(4达因/平方厘米)或动脉水平(25达因/平方厘米)的稳定层流切应力下1小时。通过免疫细胞化学和定量荧光视频显微镜测量细胞内c-fos蛋白。与维持在静止培养中的细胞相比,暴露于动脉水平切应力的细胞中核定位的c-fos蛋白水平高5.4±2.0倍(p<0.01)。相反,暴露于低水平切应力的细胞显示c-fos水平呈弥漫性但略有升高(比对照高2.4±0.73倍;p<0.01),且无优先核定位。蛋白激酶C抑制剂H7(10微摩尔)显著减弱了暴露于动脉切应力1小时的细胞中c-fos的诱导,减弱程度达50%。

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