摘要
目的炎症反应被认为是动脉粥样硬化的始动环节,也是防止动脉粥样硬化的重要靶点。众多基因参与调控此过程,PPARβ/δ可通过参与炎症反应从而影响动脉粥样硬化。我们通过生物信息学分析发现lncRNA AL110200可能影响PPARβ/δ的表达,从而我们推测lncRNA AL110200可能通过调节PPARβ/δ表达从而影响动脉粥样硬化炎症反应。本研究旨在通过体外实验研究lncRNA AL110200对炎症刺激物脂多糖的应答并初步验证其靶基因。方法我们首先使用qRT-PCR检测在炎症刺激物脂多糖(LPS)刺激下lncRNA AL110200表达量的改变;然后我们再利用qRT-PCR检测了lncRNA AL110200干扰和过表达后PPARβ/δmRNA表达水平的改变。结果我们研究发现LPS可上调lncRNA AL110200(1.85倍,P<0.001)和PPARβ/δ(2.67倍,P<0.01)表达;但是无论高表达还是低表达lncRNA AL110200都不影响PPARβ/δ的表达。结论综上所述,我们的研究发现,动脉粥样硬化炎症刺激物LPS可以上调lncRNA AL110200及PPARβ/δ表达,但是PPARβ/δ非lncRNA AL110200的靶基因。
Objective Inflammation caused by monocytes migration to vascular intima is the first step in atherogenesis, which is important target of prevention of atherosclerosis. This process is regulated by many genes, including PPAR β/δ, which are associated with inflammation of atherosclerosis. Based on analysis results of bioinformation, we presumed that incRNA AL 110200 may regulate the expression of PPAR β/δ In our study, we aimed to explore the response to LPS and the target gene of IncRNA AL110200 in vitro. Methods We performed QRT-PCR analysis to examine the expression of lncRNA AL 110200 in THP-1 cells treated with LPS. And then we use qRT-PCR to test the expression of PPAR β/δ in THP-1 cells with downregulation and up-regulation of lncRNAAL110200. Results Increased expression levels of lncRNA AL110200 and PPAR β/δ were observed in THP- 1 cells under LPS （1.85-fold, P〈0.001 and 2.67-fold, P〈0.01, respectively）. But no changes in expressions of PPAR β/δ were obesereed in THP-1 cells with low expression and high expression of IncRNA AL110200, respectively. Conclusion Our results indicate that the incRNA AL110200 promote inflammation of atherosclerosis, with no association with the expression of PPARβ/δ.
出处
《中国分子心脏病学杂志》
CAS
2013年第5期682-685,共4页
Molecular Cardiology of China
基金
国家自然科学基金(81270356)
