Benzo[a]pyrene Potentiates the Pathogenesis of Abdominal Aortic Aneurysms in Apolipoprotein E Knockout Mice
| Autor: | Petra Prins, Valentina Kon, Aramandla Ramesh, ZhongMao Guo, Uchechukwu K.A. Sampson, Sergio Fazio, MacRae F. Linton, Prudhvidhar R. Perati |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Apolipoprotein E
Male medicine.medical_specialty animal structures Physiology Inflammation complex mixtures Pathogenesis chemistry.chemical_compound Mice Apolipoproteins E medicine.artery Internal medicine medicine polycyclic compounds Benzo(a)pyrene Animals Aorta Mice Knockout Original Paper business.industry Tumor Necrosis Factor-alpha Angiotensin II Macrophages Anatomy Mice Inbred C57BL Endocrinology chemistry Matrix Metalloproteinase 9 Knockout mouse cardiovascular system Tumor necrosis factor alpha medicine.symptom business Cyclophilin A hormones hormone substitutes and hormone antagonists Aortic Aneurysm Abdominal |
| Popis: | The objective of this study was to determine the effect of benzo[a]pyrene (BaP), an abundant environmental polycyclic aromatic hydrocarbon compound, on the pathogenesis of abdominal aortic aneurysms (AAA). Earlier studies have shown that BaP promotes vasculopathy, including atherosclerosis, a predisposing factor for AAA development. In two experimental arms, 203 apolipoprotein E knockout (ApoE-/-) mice were evaluated in 4 groups: BaP, angiotensin II (AngII), BaP+AngII and control. Mice in the first arm were exposed to 5mg/kg/week of BaP for 42 days, and in the second arm to 0.71mg/kg daily for 60 days. In arm one, AAA incidence was higher in the BaP+AngII (14/28) versus AngII (8/27) group (p < 0.05), rupture (n=3) was observed only in BaP+AngII treated mice (p < 0.05). In the second arm, AAA incidence did not differ between AngII (17/30) and BaP+AngII (16/29) groups. However, intact AAA diameter was larger in the BaP+AngII (2.3 ± 0.1mm) versus AngII (1.9 ± 0.1mm) group (p < 0.05), but AAA rupture did not differ (p=NS). In both experimental arms, BaP+AngII mice showed increased expression of tumor necrosis factor alpha (TNF-α), cyclophilin A (Cyp A), and matrix metalloproteinase-9 (MMP9) (p < 0.05). No AAA occurred in control or BaP groups. These findings suggest the role of BaP exposure in potentiating AAA pathogenesis, which may have potential public health significance. |
| Databáze: | OpenAIRE |
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