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Table 2 Animal studies on the association between PM2.5 exposure and atherosclerosis

From: The critical role of endothelial function in fine particulate matter-induced atherosclerosis

Reference

PM2.5 source

Mouse model

Diet

Exposure

Time

Findings

[94]

Shanghai, China

Ambient PM2.5

ApoE-/- mice

Normal chow; High-fat diet

8 h/day,

7 days/week,

16 weeks

PM2.5 exposure induced and promoted atherosclerotic lesions with significant difference.

Increased:

Atherosclerotic plaque; lipids (ApoB, LDL-C, T-CHO, TG); CD36; ox-LDL; inflammatory cytokines (IL-1β, IL-18); NLRP3, caspase-1, ASC, pro-caspase-1, cleaved-caspase-1;

Decreased:

Lipids (ApoA1 and HDL-C)

[95]

Nanjing, China

Ambient PM2.5

ApoE-/- mice

High-fat diet

12 weeks

PM2.5 exposure amplified atherosclerotic lesions with significant difference.

Increased:

Atherosclerotic plaque; lipid accumulation; TC; LDL-C; Inflammatory cytokines (IL-6, TNF-α);

Deceased:

Anti-inflammatory cytokines (IL-10, TGF-β); CD4+CD25+Foxp3+Tregs; Foxp3

[96]

Beijing, China

Ambient PM (PM2.5 and PM10)

ApoE-/- mice

High-fat diet

24 h/day,

7 days/week,

2 months

PM2.5 increased atherosclerotic plaque with significant difference.

Increased:

Lesion area; TC; LDL; ox-LDL; visfatin; systemic inflammation and pulmonary inflammation response (IL-6, TNF-α); MDA

Decreased:

SOD; GSH-Px

[97]

Beijing, China

Ambient PM (PM2.5 and PM10)

ApoE-/- mice

High-fat diet

24 h/day,

7 days/week,

2 months

PM2.5 exposure increased atherosclerotic plaque with significant difference.

Increased:

Plaque area; TC; LDL; ox-LDL; systemic inflammation (Hs-CRP, IL-6, TNF-α) and pulmonary inflammation response (IL-6, TNF-α);

Decreased:

T-AOC; SOD

[12]

Michigan State University, USA

Ambient PM2.5

ApoE-/- or LDLR-/- mice

High-fat diet

6 h/day,

5 days/week,

6 months

PM2.5 exposure increased atherosclerotic plaque with significant difference.

Increased:

Lesion area; lipid and collagen content; 7-KCh and uptake; CD36; foam cell formation

[51]

Nanjing, China Ambient PM2.5

ApoE-/- mice

High-fat diet

twice/week,

12 weeks or 24 weeks

PM2.5 exposure promoted atherosclerotic plaque development and increased plaque vulnerability, with significant difference.

Increased:

Lesion area, lipid; broken aortic elastic fibers;

Decreased:

Collagen content; fibrous cap

[6]

Beijing, China

Ambient PM2.5

ApoE-/- mice

High-fat diet

Every 3 days,

2 months,

PM2.5 exposure increased the formation of atherosclerosis and the influence probably persisted after 1-month recovery, with significant difference.

Increased:

Atherosclerotic lesion; inflammatory cytokines; lipid metabolism alteration.

[98]

Tianjin, China

Traffic related PM2.5, simulated PM2.5

ApoE-/- mice

High-fat diet

Every two days, 10 weeks

Traffic related and simulated PM2.5 promoted the formation of atherosclerosis with significant difference.

Increased:

Plaque; T-CHO; LDL-C; TG; MDA;

Decreased:

HDL-C; SOD; GSH-Px

[99]

Northeastern,

China

Ambient PM2.5, WDE, DEG

ApoE-/-

mice

Normal chow

average of 5.2 hours/day, 4 days/week, 3 months and 5 months

Exposure to PM2.5 for 5 months induced atherosclerotic plaques with significant difference.

For plaque exacerbation, PM2.5 > WDE > DEG = FA

Increased:

Plaque; vasomotor dysfunction; inflammation

[100]

Yinchuan, China coal-fired PM2.5

C57BL/6J mice and ApoE-/- mice

High-fat diet

3 h/day,

1 day/week,

8 weeks

Coal-fired PM2.5 significantly promoted the formation atherosclerosis with significant difference.

Increased:

Plaque; foam cells; fibrous cap formation; ET-1; ICAM-1; E-selectin

Decreased:

vWF

[101]

Manhattan,

USA

PM2.5

ApoE-/- mice

Normal chow and High-fat diet

6 h/day,

5 day/week,

6 months

In high-fat diet group, PM2.5 increased plaque area compared with FA (p < 0.01);

In normal chow group, PM2.5 increased plaque area compared with FA (p < 0.15).

Increased:

Plaque area; Cholesterol; Constriction response; CD68; 3-Nitrotyrosine; eNOS; iNOS;

Decreased:

Relaxation response

[102]

Los Angeles freeway, USA

PM2.5

ApoE-/- mice

regular diet

5 h/day,

3 day/week,

75 hours

PM2.5 resulted in aortic atherosclerotic lesion increased trend (p = 0.1).

Increased:

Plaque area; Liver MDA;

Decreased:

HDL anti-inflammatory properties

[103]

New York; USA

PM2.5

C57BL/6, ApoE-/- mice, ApoE and LDLR double knockout (DK)

High-fat diet and regular diet

6 h/day,

5 day/week,

5 months

PM2.5 exposure increased atherosclerotic lesion in ApoE-/- mice (p < 0.05).

Atherosclerotic lesion 57% increase in ApoE-/- mice; Atherosclerotic lesion 10% increase in male DK mice and 8% decrease in female DK mice.

[104]

New York; USA

PM2.5

ApoE-/- mice

High-fat diet

30 mg/kg/day, 8 weeks

PM2.5 contributed to the progression of atherosclerosis (p < 0.05).

Increased:

Atherosclerotic plaques; numbers of lesion macrophages; endothelial layer injury; platelets and leukocytes adherence; IL-6; TNF-α; iNOS; IL-12; arginase-1; CD206

[26]

DEP, 1650b, NIST, USA

C57BL/6,

ApoE-/- mice

Regular chow or high-fat diet

Once a day during 5 days/week, 3-6 weeks

DEP exposure increased atherosclerotic lesion in ApoE-/- mice (p < 0.05).

Increased:

Atherosclerotic plaques; EPC apoptosis; superoxide production;

Decreased:

Neoangiogenesis; EPC migration; Endothelial cell interity

[25]

DEP, SRM-2975, NIST, USA

C57BL/6,

ApoE-/- mice

Regular chow or high-fat diet

Twice weekly instillation

DEP exposure increased atherosclerotic lesion in ApoE-/- mice (p < 0.05).

Increased:

Atherosclerotic plaques; Cholesterol; antioxidant genes in the liver

  1. Note: Apo A1 apolipoprotein A1, Apo B apolipoprotein B, ASC apoptosis associated speck like protein, CD36 cluster of differentiation 36, DEG diesel exhaust gases, DEP Diesel exhaust particles, ET-1 endothelin-1, eNOS endothelial nitric oxide synthase, FA filtered air, Foxp3 forkhead box transcription factor P3, GSH-Px glutathione peroxidase, HDL-C high density lipoprotein-cholesterol, Hs-CRP high sensitive C-reactive protein, IL interleukin, ICAM-1 Intercellular Adhesion Molecule-1, iNOS inducible nitric oxide synthase, 7-KCh 7-ketocholesterol, LDL-C low density lipoprotein-cholesterol, MDA malondialdehyde, NIST National Institute of Standards and Technology, NLRP3 NOD-like receptor protein 3, ox-LDL oxidized low-density lipoprotein, PM particulate matter, SOD superoxide dismutase, T-AOC total antioxidant capacity, T-CHO total cholesterol, TG triglycerides, TGF-β transforming growth factor-β, TNF-α tumor necrosis factor α, vWF von willebrand factor, WDE whole diesel exhaust