Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice by upregulating visfatin expression

Abstract

Ambient particulate matter (PM) exposure has been associated with atherosclerosis. However, research on the effect of real-world exposure to ambient PM in regulating visfatin expression in an animal model is very limited. The objective is to investigate whether Beijing ambient PM exposure could accelerate atherosclerosis in ApoE knockout (ApoE(-/-)) mice by upregulating visfatin expression. Forty male ApoE(-/-) mice were exposed to untreated ambient air (PM group, n = 20) or filtered air (FA group, n = 20), 24 h/day, 7 days/week, for 2 months. During the exposure, the mass concentrations of PM2.5 and PM10 in the two groups were continuously monitored. Moreover, a receptor source apportionment model was applied to apportion sources of PM2.5. At the end of the exposure, visfatin in plasma and aorta, biomarkers of inflammation, oxidative stress and lipid metabolism in blood samples, and bronchoalveolar lavage fluid (BALF) were determined, and the plaque area of the atherosclerosis lesions was quantified. PM-exposed mice were significantly higher than FA-exposed mice in terms of plasma visfatin, OxLDL, MDA, serum TC, LDL, TNF-α as well as IL-6, TNF-α, OxLDL, and MDA in BALF, while SOD and GSH-Px activities in plasma and BALF were reduced in PM-exposed mice. Pathological analysis of the aorta demonstrated that the plaque area and visfatin protein in the PM group increased significantly compared to the FA group. Our findings indicate that ambient PM exposure could accelerate atherosclerosis, which is related to visfatin upregulation, as well as the activation of inflammation and oxidative stress.

Tubeimoside I attenuates inflammation and oxidative damage in a mice model of PM2.5‑induced pulmonary injury

“…PM with an aerodynamic diameter <2.5 µm (PM 2.5 ) is the primary PM pollutant. Sources of PM 2.5 include toxic organic compounds, heavy metals, the burning of plant material and forest fires (4). PM 2.5 is easily inhaled into the airway and deposited in lung alveoli, where the toxic particles may affect pulmonary structures and functions.…”

Effects of urban fine particulate matter and ozone on HDL functionality

“…Exposure to ambient PM 2.5 (PM <2.5 μm) has been associated with the development of atherosclerosis [ 3 – 6 ] and the rate of carotid intima-media thickness (CIMT) progression over time [ 7 , 8 ]. Similarly, sub-chronic exposure studies in animals have shown that apolipoprotein E (ApoE) null mice exposed to PM at ambient levels [ 9 , 10 ], concentrated PM 2.5 [ 11 , 12 ], ultrafine particles (UFP) [ 13 ], and diesel exhaust emissions [ 14 ], show accelerated atherosclerosis. ApoE null [ 15 ] and low density lipoprotein-receptor (LDL-R) null mice [ 16 ] exposed to intratracheal particulate, devoid of gases, also display increased severity and complexity of atherosclerotic plaques.…”

Exposure to concentrated ambient fine particulate matter disrupts vascular endothelial cell barrier function via the IL‐6/HIF‐1α signaling pathway

“…Our findings indicate that concentrated PM2.5 can destroy membrane integrity and promote permeability in vascular endothelial cells, thereby contributing to the development of CVDs.There is increasing concern about the potential deleterious effects of ambient air pollution, which is currently recognized as a significant risk to global public health. A growing body of epidemiological and clinical research data have demonstrated that short-and long-term exposure to ambient particulate matter less than 2.5 lm in aerodynamic diameter (PM2.5, fine particles) is linked to an increase in cardiovascular disease (CVD), morbidity and mortality, particularly in accelerating atherosclerosis (AS) development [1][2][3][4][5]. Several recent reports provide experimental evidence that demonstrates that the translocation of PM2.5 from the lung and directly into the blood exacerbates the progression of AS by initiating acute inflammatory responses [6][7][8].…”