层流切应力通过 NADPH 氧化酶 2 依赖性机制增强内皮细胞的存活。
Laminar shear stress enhances endothelial cell survival through a NADPH oxidase 2-dependent mechanism.
机构信息
Department of Molecular Medicine, Cell and Matrix Research Institute, BK21 Medical Education Program for Human Resources, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
出版信息
Biochem Biophys Res Commun. 2013 Jan 11;430(2):460-5. doi: 10.1016/j.bbrc.2012.12.016. Epub 2012 Dec 10.
The beneficial effects of laminar shear stress (LSS) due to blood flow include inhibition of endothelial cell death, but the associated mechanism is not well understood. This issue was addressed in the present study. In a normal growth medium, the endothelial cell death rate was below 5%, but this value increased beyond 30% when the serum was depleted. However, when cells were exposed to LSS during the serum depletion period, cell viability recovered to the levels of the serum-provided cells. The pro-survival effect of LSS was not affected by l-arginine methyl ester, but it was abrogated by apocynin, indicating that NADPH oxidases (NOX) play key roles in the mechanism. The pro-survival effect of LSS was reduced by NOX2 siRNA, but not by NOX4 siRNA. LSS increased the expressions of p47(phox) and p67(phox), the subunits of NOX2 complex. These observations suggest that LSS prevents apoptotic death of endothelial cells through a NOX2-dependent mechanism.
层流剪切应力（LSS）对血流的有益影响包括抑制内皮细胞死亡，但相关机制尚不清楚。本研究探讨了这一问题。在正常生长培养基中，内皮细胞的死亡率低于 5%，但当血清耗尽时，这一数值会增加到 30%以上。然而，当细胞在血清耗竭期间暴露于 LSS 时，细胞活力恢复到有血清提供的细胞的水平。LSS 的促生存作用不受 l-精氨酸甲酯的影响，但被 apocynin 阻断，表明 NADPH 氧化酶（NOX）在该机制中起关键作用。LSS 的促生存作用被 NOX2 siRNA 降低，但不受 NOX4 siRNA 的影响。LSS 增加了 NOX2 复合物的亚基 p47(phox)和 p67(phox)的表达。这些观察结果表明，LSS 通过一种依赖于 NOX2 的机制防止内皮细胞凋亡性死亡。
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