Abstract

Researches have demonstrated that trans-fatty acids are related to the progression of atherosclerosis, but the underlying mechanism is not clear till now. In the presented study, two-dimensional electrophoresis based proteomics was used to discover the role of elaidic acid in atherosclerosis. In human umbilical vein endothelial cells (HUVEC), twenty-two and twenty-three differentially expressed proteins were identified in low (50 μmol/L) and high (400 μmol/L) concentration elaidic acid simulated groups, respectively, comparing with the control group. The expressions of some selected proteins (PSME3, XRCC5, GSTP1, and GSTO1) were validated by qRT-PCR analysis. Western blotting analysis further confirmed that elaidic acid downregulated the expression of PSME3and XRCC5. Moreover, P53, the downstream protein of PSME3, was further investigated. Results demonstrated that a variety of proteins, many of which were related to oxidative stress, apoptosis, and DNA damage, were involved in the elaidic acid induced atherosclerosis. Furthermore, P53 was demonstrated to regulate the atherosclerosis through cell cycle arrest and apoptosis pathway.

Highlights

  • Trans-fatty acids (TFA) refer to unsaturated fatty acids that contain at least one double bond in the trans-configuration [1]

  • The two-dimensional electrophoresis- (2-DE-) based proteomics was used to detect these proteins related to elaidic acid induced AS

  • The viabilityof human umbilical vein endothelial cells (HUVEC) treated with different concentrations of elaidic acid for 48 h was examined by MTT assays

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Summary

Introduction

Trans-fatty acids (TFA) refer to unsaturated fatty acids that contain at least one double bond in the trans-configuration [1]. TFA is considered to be correlated positively with coronary heart disease, especially atherosclerosis (AS) [3]. Those countries with high TFA intake, such as Northern European countries, had higher coronary heart disease [4]. Fischer et al found that diet containing linolelaidic acid would increase the proportion of LDL/HDL by 8.1% [5]. Another TFA, elaidic acid, could influence arachidonic acid metabolism, playing an important role in formation of athermanous plaque [6]

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