Depletion of CPEB1 protects against oxidized LDL-induced endothelial apoptosis and inflammation though SIRT1/LOX-1 signalling pathway.
作者： Kaicheng Xu , Xiwen liu , Guanghao Ren , Dexin Yin , Suli Guo
DOI: 10.1016/J.LFS.2019.116874
关键词: Chemistry 、 Inflammation 、 Apoptosis 、 Transcription (biology) 、 Cell biology 、 Sirtuin 1 、 Oxidative stress 、 Kinase 、 Small interfering RNA 、 RNA
摘要: Atherosclerosis (AS) is a chronic inflammatory disease that results from Oxidized low-density lipoprotein (Ox-LDL) induced endothelial dysfunction. Cytoplasmic polyadenylation element binding protein 1 (CPEB1) closely related to the development of epithelial cells, but role CPEB1 in AS remains unknown. The RNA and levels expression are increased by Ox-LDL exposure, which abrogated c-Jun amino-terminal kinase (JNK) inhibitor SP600125. small interfering (siRNA) suppressed oxidative stress, inflammation, apoptosis. Furthermore, siRNA enhanced sirtuin (SIRT1) transcription Ox-LDL-treated HUVECs. Co-Immunoprecipitation (Co-IP) assay showed declined ubiquitination SIRT1, SIRT1 Lectin-like oxidized receptor-1 (LOX-1), were decreased siRNA. In addition, LOX-1 attenuated protection on Ox-LDL-induced stress. Therefore, our study revealed depletion might play an anti-inflammatory antiapoptotic apoptosis inflammation though SIRT1/LOX-1 signalling pathway.
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