磷脂酰乙醇胺结合蛋白 1 在血管内皮细胞自噬和动脉粥样硬化中的作用。
Phosphatidylethanolamine binding protein 1 in vacular endothelial cell autophagy and atherosclerosis.
机构信息
J. Y. Miao and B. X. Zhao: Institute of Developmental Biology, School of Life Science, Shandong University, Jinan 250100, China. Emails:
出版信息
J Physiol. 2013 Oct 15;591(20):5005-15. doi: 10.1113/jphysiol.2013.262667. Epub 2013 Aug 19.
Abstract
We previously found that phosphatidylcholine-specific phospholipase C (PC-PLC) was a key inducing element of atherosclerosis, and might negatively regulate human umbilical vein endothelial cell (HUVEC) autophagy. To further investigate the mechanism of PC-PLC action, we initially identified phosphatidylethanolamine binding protein 1 (PEBP1) as a binding partner of PC-PLC by using mass spectrometry (MS, MALDI-TOF/TOF). We found that PEBP1 positively regulated PC-PLC activity in HUVECs, and inhibition of PC-PLC by its inhibitor D609 suppressed PEBP1 expression dramatically. Moreover, both PC-PLC and PEBP1 negatively regulated HUVEC autophagy independently of mammalian target of rapamycin (mTOR). Furthermore, the PEBP1 level was elevated during the development of atherosclerosis, while D609 significantly decreased the upregulated PEBP1 level in apoE(-/-) mice.
摘要
我们之前发现磷脂酰胆碱特异性磷脂酶 C（PC-PLC）是动脉粥样硬化的关键诱导因子，可能负向调节人脐静脉内皮细胞（HUVEC）自噬。为了进一步研究 PC-PLC 的作用机制，我们最初通过质谱（MS，MALDI-TOF/TOF）鉴定出磷脂酰乙醇胺结合蛋白 1（PEBP1）是 PC-PLC 的结合伴侣。我们发现 PEBP1 可正向调节 HUVEC 中的 PC-PLC 活性，而其抑制剂 D609 可显著抑制 PC-PLC 的活性，从而抑制 PEBP1 的表达。此外，PC-PLC 和 PEBP1 均独立于雷帕霉素靶蛋白（mTOR）负向调节 HUVEC 自噬。此外，PEBP1 水平在动脉粥样硬化的发展过程中升高，而 D609 可显著降低 apoE(-/-) 小鼠中上调的 PEBP1 水平。
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