血流动力学因素在动脉粥样硬化的发生和发展中起关键作用。血管内皮细胞（ECs）是血流切应力的作用对象，我们的前期研究表明非编码RNA参与介导了切应力对ECs炎症的调控。然而，目前非编码RNA的研究多数集中在microRNA领域，针对长链非编码RNA（lncRNA）家族中高度保守的T-UCR是否参与介导切应力对ECs炎症的调控仍不清楚。我们的lncRNA芯片结果显示：不同的切应力环境下，ECs拥有不同lncRNA表达谱。与抗炎的生理切应力比较，促炎的低切应力诱导uc.234-和uc.351-的表达发生了最显著的改变。这提示T-UCR可能参与切应力对ECs炎症的调控。本项目拟运用表达谱芯片及转基因动物实验等方法，深入探讨切应力敏感T-UCR对ECs炎症的调控作用，明确其分子机制和对动脉粥样硬化的影响。本研究有助于进一步阐明血流切应力调控ECs炎症的新机制，为动脉粥样硬化的防治提供新的理论依据。

Hemodynamic factors play a major role in the initiation and progression of atherosclerosis. Vascular endothelial cells (ECs) are continuously exposed to hemodynamic shear stress. Our preliminary studies show that non-coding RNA modulates flow-dependent regulation of endothelial inflammation. However, most studies investigating non-coding RNAs have focused on microRNAs (miRNAs), it remains unclear that whether long non-coding RNAs (lncRNAs), especially T-UCRs (transcribed ultraconserved regions) which are highly conserved in the lncRNAs family, are involved in flow-mediated regulation of endothelial inflammation. Our lncRNA microarray data show that, ECs subjected to different flow condition have distinct lncRNA expression profiles. Compared to anti-inflammatory physiological shear stress, pro-inflammatory low shear stress induces the most significantly uc.234- upregulation and uc.351- downregulation, respectively. These results suggest that T-UCRs may be involved in flow-mediated regulation of ECs inflammation. Based on these preliminary results, our present study is conducted to further investigate whether these T-UCRs can modulate endothelial inflammation, to elucidate their molecular mechanism and analysis their impact on atherosclerosis, by using microarray-based transcription profiling analysis and transgenic animal technology. The results will reveal a new mechanism by which shear stress regulates endothelial inflammation, and will provide theoretical guidance for the prevention and treatment of atherosclerosis.