PM2.5 promotes abdominal aortic aneurysm formation in angiotensin Ⅱ-infused apoe-/- mice

Biomed Pharmacother. 2018 Aug:104:550-557. doi: 10.1016/j.biopha.2018.04.107. Epub 2018 May 25.

Abstract

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.

Keywords: Abdominal aortic aneurysm; Air pollution; PM2.5; Senescence; Smooth muscle cell.

MeSH terms

  • Angiotensin II / metabolism*
  • Animals
  • Aorta, Abdominal / drug effects*
  • Aorta, Abdominal / metabolism
  • Aortic Aneurysm, Abdominal / chemically induced*
  • Aortic Aneurysm, Abdominal / metabolism
  • Apolipoproteins E / metabolism*
  • Biomarkers / metabolism
  • Cell Line
  • Chemokine CCL2 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Disease Models, Animal
  • Elastin / metabolism
  • Humans
  • Matrix Metalloproteinase 2 / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Myocytes, Smooth Muscle / drug effects
  • Myocytes, Smooth Muscle / metabolism
  • Particulate Matter / adverse effects*
  • Reactive Oxygen Species / metabolism
  • beta-Galactosidase / metabolism

Substances

  • Apolipoproteins E
  • Biomarkers
  • Chemokine CCL2
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • Particulate Matter
  • Reactive Oxygen Species
  • Angiotensin II
  • Elastin
  • beta-Galactosidase
  • Matrix Metalloproteinase 2