loading page

Atorvastatin inhibits inflammation through the cysteine-rich motor neuron 1 (Crim1) pathway in human umbilical vein endothelial cells
  • +9
  • Xuehui Liu,
  • Changmeng Wu,
  • Shuyuan Wang,
  • Xianhui Dong,
  • Xueheng Li,
  • Yanrou Bei,
  • Yu Song,
  • Limei Wu,
  • Huasen Liu,
  • Dabin Liu,
  • Shaoguo Wu,
  • Yanwei Hu
Xuehui Liu
Guangzhou Twelfth Peopls' Hospital
Author Profile
Changmeng Wu
Southern Medical University Nanfang Hospital
Author Profile
Shuyuan Wang
Haizhu Maternal and Child Health Hospital
Author Profile
Xianhui Dong
Guangzhou Women and Children’s Medical Center
Author Profile
Xueheng Li
Southern Medical University Nanfang Hospital
Author Profile
Yanrou Bei
Southern Medical University Nanfang Hospital
Author Profile
Yu Song
Southern Medical University Nanfang Hospital
Author Profile
Limei Wu
Guangzhou Twelfth People’s Hospital
Author Profile
Huasen Liu
Guangzhou Twelfth People’s Hospital
Author Profile
Dabin Liu
Guangzhou Twelfth People’s Hospital
Author Profile
Shaoguo Wu
Guangzhou Twelfth People’s Hospital

Corresponding Author:[email protected]

Author Profile
Yanwei Hu
Southern Medical University Nanfang Hospital
Author Profile

Abstract

Background and AIMS: Inflammation has been recognized to have a role in the process of atherosclerosis. Although evidence indicates that atorvastatin has anti-inflammatory effects besides cholesterol-lowering ability in atherosclerosis, the specific mechanisms of atorvastatin in inflammation requires further discussion. METHODS: Here, we explored the effects and mechanisms of atorvastatin on inflammation in human umbilical vein endothelial cells through quantitative real-time PCR and western blot analyses. In addition, microarray analysis and immunohistochemistry were used to analyze the expression of Crim1 in atherosclerotic plaques. RESULTS: Cysteine-rich motor neuron 1 (Crim1) mRNA was upregulated 36.68 fold (P<0.001), and Crim1 protein was upregulated 3.63 fold (p<0.001), in human atherosclerotic plaques compared with normal intima tissues. Bioinformatics analysis revealed Crim1 co-expression with IL-6, TNF-α and NF-κB. Atorvastatin dramatically downregulated the mRNA and protein levels of Crim1 and inhibited inflammation by decreasing the levels of IL-6, TNF-α and NF-κB. Knockdown of Crim1 significantly inhibited IL-6, TNF-α and NF-κB expression, whereas overexpression of Crim1 upregulated IL-6, TNF-α and NF-κB expression. In addition, the inhibitory effects of atorvastatin on inflammation were markedly offset by overexpression of Crim1. CONCLUSION: These results demonstrated that atorvastatin decreases inflammation via the Crim1 pathway in HUVECs, thus, providing a new prospect for the use of atorvastatin for non-lipid lowering functions, and new directions for the prevention and therapy of atherosclerosis.