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Published on: September 28, 2015
PM2.5 promotes abdominal aortic aneurysm formation in angiotensin Ⅱ-infused apoe-/- mice
1Department of Cardiology, Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Background:
Particulate matter 2.5 (PM2.5) has proven to be associated with morbidity and mortality from cardiovascular diseases. However, whether PM2.5 could promote the formation of abdominal aortic aneurysm (AAA) is unclear. Present study aimed to explore the relationship between PM2.5 exposure and AAA development.
Methods:
Ang Ⅱ-infused apoe-/- mice were treated with PM2.5 or saline by intranasal instillation. Four weeks later, histological and immunohistological analyses were used to evaluate the effect of PM2.5 on AAA formation. Human aortic smooth muscle cells (HASMCs) were also employed to further analyze the adverse effect of PM2.5 in vitro.
Results:
We found that PM2.5 could significantly increase the AAA incidence, the maximal abdominal aortic diameter and could promote the degradation of elastin. Additionally, the expression of senescence markers, P21 and P16 were also enhanced after PM2.5 exposure. We also found that PM2.5 significantly increased the AAA related pathological changes, MMP2 and MCP-1 expression in HASMCs. Meanwhile, PM2.5 could increase the expression of senescence markers P21, P16 and SA-β-gal activity, also the reactive oxygen species levels in vitro.
Conclusions:
PM2.5 promoted the formation of AAA in an Ang Ⅱ-induced AAA model. The underlying mechanism might be cellular senescence after PM2.5 exposure.
Insights
Exposure to fine particulate matter (PM2.5) significantly promotes abdominal aortic aneurysm (AAA) development in mice. This may be linked to PM2.5-induced cellular senescence, highlighting a new cardiovascular risk factor.
Area of Science:
- Environmental Health
- Cardiovascular Research
- Toxicology
Background:
- Particulate matter 2.5 (PM2.5) is linked to cardiovascular disease mortality.
- The role of PM2.5 in abdominal aortic aneurysm (AAA) formation is not well understood.
Purpose of the Study:
- To investigate the association between PM2.5 exposure and the development of AAA.
- To elucidate the potential mechanisms underlying PM2.5-induced AAA.
Main Methods:
- Angiotensin II-infused apolipoprotein E-deficient mice were exposed to PM2.5 or saline via intranasal instillation.
- Histological and immunohistological analyses were performed to assess AAA formation and related markers.
- Human aortic smooth muscle cells (HASMCs) were used for in vitro mechanistic studies.
Main Results:
- PM2.5 exposure significantly increased AAA incidence, aortic diameter, and elastin degradation.
- PM2.5 enhanced the expression of senescence markers (P21, P16), MMP2, MCP-1, and reactive oxygen species in vitro.
- Cellular senescence was identified as a potential mechanism in PM2.5-induced AAA.
Conclusions:
- PM2.5 promotes AAA formation in a mouse model.
- Cellular senescence induced by PM2.5 exposure is a likely underlying mechanism for AAA development.
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