NDLI: Atorvastatin up-regulates TRIB3 independent of ATF4-CHOP pathway in atherosclerotic patients

Content Provider	PubMed Central
Author	Bi, Shao-jie Wang, Chun-yan Zhang, Juan Lv, Zhao-peng Li, Yi-xin
Copyright Year	2015
Abstract	Background: Macrophage apoptosis triggered by endoplasmic reticulum (ER) stress contributes much to atherosclerosis, especially plaque vulnerability. Activating transcription factor 4 (ATF4)-CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP)-Tribbles 3 (TRIB3) pathway is closely related to the ER stress. This study aimed to investigate the effect of atorvastatin on the ATF4-CHOP-TRIB3 pathway. Methods: Forty-seven patients were randomized into 80-mg and 20-mg atorvastatin group. Follow-up was performed at weeks 6 and 12, and complete blood chemistry, lipid assay and detection of 5 target genes (tumor protein 53, ATF4, C/EBP, CHOP and TRIB3) in monocytes/macrophages were conducted. Furthermore, the interaction between dosage and duration of therapy was evaluated. Results: After 12-week therapy, patients in both groups experienced significant reductions in ATF4 (P=0.038) and C/EBP (P=0.003) expressions. Tumor protein 53 (P=0.015) and TRIB3 (P=0.045) expressions increased markedly in 80-mg atorvastatin group. However, there was no significant difference in CHOP expression at three time-points and between atorvastatin groups. Moreover, there was no interaction between dosage and duration of therapy. Conclusions: Atorvastatin has an effect on ER stress through ATF4-CHOP pathway. Atorvastatin at a high dose is more likely to increase TRIB3 expression, but this warrants further investigation.
Ending Page	21640
Starting Page	21635
File Format	PDF
ISSN	19405901
e-ISSN	19405901
Journal	International Journal of Clinical and Experimental Medicine
Issue Number	11
Volume Number	8
Language	English
Publisher	e-Century Publishing Corporation
Publisher Date	2015-11-15
Access Restriction	Open
Rights Holder	e-Century Publishing Corporation
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Biochemistry, Genetics and Molecular Biology

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