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Tytuł pozycji:

Depletion of CPEB1 protects against oxidized LDL-induced endothelial apoptosis and inflammation though SIRT1/LOX-1 signalling pathway.

Tytuł:
Depletion of CPEB1 protects against oxidized LDL-induced endothelial apoptosis and inflammation though SIRT1/LOX-1 signalling pathway.
Autorzy:
Xu K; Department of Anesthesiology, China-Japan Union Hospital JiLin University, Chang Chun, JiLin, 130033, China.
Xiwen Liu; Department of Vascular Surgery, China-Japan Union Hospital JiLin University, Chang Chun, JiLin, 130033, China.
Ren G; Department of Vascular Surgery, China-Japan Union Hospital JiLin University, Chang Chun, JiLin, 130033, China.
Yin D; Department of Vascular Surgery, China-Japan Union Hospital JiLin University, Chang Chun, JiLin, 130033, China.
Guo S; Department of Vascular Surgery, China-Japan Union Hospital JiLin University, Chang Chun, JiLin, 130033, China.
Zhao Y; Department of Vascular Surgery, China-Japan Union Hospital JiLin University, Chang Chun, JiLin, 130033, China. Electronic address: .
Źródło:
Life sciences [Life Sci] 2019 Dec 15; Vol. 239, pp. 116874. Date of Electronic Publication: 2019 Sep 12.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
MeSH Terms:
Scavenger Receptors, Class E/*metabolism
Sirtuin 1/*metabolism
Transcription Factors/*deficiency
mRNA Cleavage and Polyadenylation Factors/*deficiency
Apoptosis/physiology ; Atherosclerosis/metabolism ; Atherosclerosis/physiopathology ; Endothelium/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Inflammation/metabolism ; Lipoproteins, LDL/metabolism ; Oxidative Stress/drug effects ; Signal Transduction ; Transcription Factors/metabolism ; mRNA Cleavage and Polyadenylation Factors/metabolism
Contributed Indexing:
Keywords: CPEB1; Endothelial dysfunction; Inflammation; LOX-1; Oxidized LDL
Substance Nomenclature:
0 (CPEB1 protein, human)
0 (Lipoproteins, LDL)
0 (OLR1 protein, human)
0 (Scavenger Receptors, Class E)
0 (Transcription Factors)
0 (mRNA Cleavage and Polyadenylation Factors)
0 (oxidized low density lipoprotein)
EC 3.5.1.- (SIRT1 protein, human)
EC 3.5.1.- (Sirtuin 1)
Entry Date(s):
Date Created: 20190916 Date Completed: 20200213 Latest Revision: 20200213
Update Code:
20240105
DOI:
10.1016/j.lfs.2019.116874
PMID:
31521690
Czasopismo naukowe
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) is closely related to the development of epithelial cells, but the role of CPEB1 in AS remains unknown. The RNA and protein levels of CPEB1 expression are increased by Ox-LDL exposure, which is abrogated by c-Jun amino-terminal kinase (JNK) inhibitor SP600125. CPEB1 small interfering RNA (siRNA) suppressed the oxidative stress, inflammation, and apoptosis. Furthermore, CPEB1 siRNA enhanced the sirtuin 1 (SIRT1) transcription levels in Ox-LDL-treated HUVECs. Co-Immunoprecipitation (Co-IP) assay showed that CPEB1 siRNA declined the ubiquitination of SIRT1, and SIRT1 siRNA enhanced the Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), which were decreased by CPEB1 siRNA. In addition, LOX-1 and SIRT1 attenuated the protection of SIRT1 siRNA on Ox-LDL-induced oxidative stress. Therefore, our study revealed that CPEB1 depletion might play an anti-inflammatory and antiapoptotic role in Ox-LDL-induced apoptosis and inflammation though SIRT1/LOX-1 signalling pathway.
(Copyright © 2019 Elsevier Inc. All rights reserved.)

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