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. 2020 May 8;21(1):34.
doi: 10.1186/s40360-020-00411-8.

Effects of coal-fired PM2.5 on the expression levels of atherosclerosis-related proteins and the phosphorylation level of MAPK in ApoE-/- mice

Siqi Wang  1   2 , Feifei Wang  3 , Lixin Yang  3 , Qin Li  3 , Yao Huang  1   2 , Zhiyuan Cheng  1   2 , Hongqian Chu  1   4   5 , Yiming Song  1   2 , Lanqin Shang  1   2 , Weidong Hao  1   2 , Xuetao Wei  6   7
Affiliations

Effects of coal-fired PM2.5 on the expression levels of atherosclerosis-related proteins and the phosphorylation level of MAPK in ApoE-/- mice

Siqi Wang et al. BMC Pharmacol Toxicol. .

Abstract

Background: Air pollution increases the morbidity and mortality of cardiovascular disease (CVD). Atherosclerosis (AS) is the pathological basis of most CVD, and the progression of atherosclerosis and the increase of fragile plaque rupture are the mechanism basis of the relationship between atmospheric particulate pollution and CVD. The aim of the present study was to investigate the effects of coal-fired fine particulate matter (PM2.5) on the expression levels of atherosclerosis-related proteins (von Willebrand factor (vWF), Endothelin-1 (ET-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin, and to explore the role and mechanism of the progression of atherosclerosis induced by coal-fired PM2.5 via the mitogen-activated protein kinase (MAPK) signaling pathways.

Methods: Different concentrations of PM2.5 were given to apolipoprotein-E knockout (ApoE-/-) mice via intratracheal instillation for 8 weeks. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of vWF, ET-1 in serum of mice. Immunohistochemistry was used to observe the expression and distribution of ICAM-1 and E-selectin in the aorta of mice. Western blot was used to investigate the phosphoylation of proteins relevant to MAPK signaling pathways.

Results: Coal-fired PM2.5 exacerbated atherosclerosis induced by a high-fat diet. Fibrous cap formation, foam cells accumulation, and atherosclerotic lesions were observed in the aortas of PM2.5-treated mice. Coal-fired PM2.5 increased the protein levels of ET-1, ICAM-1, and E-selectin, but there was no significant difference in the vWF levels between the PM2.5-treatment mice and the HFD control mice. Coal-fired PM2.5 promoted the phosphorylation of p38, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) in aortic tissues of mice.

Conclusion: Coal-derived PM2.5 exacerbated the formation of atherosclerosis in mice, increased the expression levels of atherosclerosis-related proteins in mice serum, and promoted the phosphorylation of proteins relevant to MAPK signaling pathway. Thus, MAPK signaling pathway may play a role in the atherosclerosis pathogenesis induced by Coal-derived PM2.5.

Keywords: ApoE−/− mice; Atherosclerosis; Coal-fired PM2.5.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Effect of coal-fired PM2.5 on body weight (n = 8)
Fig. 2
Fig. 2
Effects of coal-fired PM2.5 on mediastinal lymph nodes in terms of (a) weight, and (b) organ coefficient (compared with HFD control mice, *P < 0.05, **P < 0.01, n = 8)
Fig. 3
Fig. 3
Histological assessment of ApoE−/− mice aortas (a) 200x magnification and (b) 400x magnification (H&E staining)
Fig. 4
Fig. 4
Effect of coal-fired PM2.5 on the levels of proteins (a) vWF, (b) ET-1, (c) ICAM-1 (the brown areas are ICAM-1-positive cells, 400x magnification), and (d) E-selectin (the brown areas are E-selectin-positive cells, 400x magnification); compared with HFD control mice, *P < 0.05, **P < 0.01, n = 8
Fig. 5
Fig. 5
Effects of coal-fired PM2.5 on MAPK signaling pathways (a) p-p38, (b) p-JNK, and (c) p-ERK (tubulin was considered as an internal control; compared with HFD control mice, *P < 0.05, **P < 0.01, n = 3)
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