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[[abstract]]Despite a protective role of the anti-oxidative and anti-inflammatory heme oxygenase-1 (HO-1) in several  cardiovascular  diseases  has  been  established,  the  role  of  HO-1  in  abdominal  aortic aneurysm (AAA) formation remains unclear. We subjected mice deficient in apoE or deficient in both HO-1 and apoE to an angiotensin II-infused AAA model. HO-1 was barely detectable in the aorta  under  normal  physiological  conditions  but  markedly  induced  in  the  aortic  wall  after angiotensin II infusion, implicating a role in AAA. HO-1 deficiency increased AAA incidence and rupture  rate,  increased  aortic  aneurysmal  area  and  severity,  accompanied  with  severe  elastin degradation  and  medial  degeneration.  Further  analysis  revealed  that  lack  of  HO-1  markedly enhanced reactive oxygen species levels, smooth muscle cell (SMC) loss, macrophage infiltration, and  matrix  metalloproteinase  (MMP)  activity  in  the  aneurysmal  aortic  wall,  resulting  in exacerbated AAA formation. In vitro, angiotensin II induced HO-1 expressions in apoE-deficient SMCs and macrophages. Deficiency in both HO-1 and apoE rendered SMCs more susceptible to oxidant-induced  cell  death,  and  an  enhanced  MMP2  activity  in  response  to  angiotensin  II.  In primary macrophages, absence of HO-1 aggravated the responses to angiotensin II by increasing inflammatory cytokine productions and MMP9 activity. Taken together, our results demonstrate that  the  induction  of  HO-1  in  the  aortic  wall  during  AAA  progression  might  be  a  protective mechanism  while  deficiency  of  HO-1  exacerbates  AAA  via  enhanced  oxidative  stress  and inflammation. Increasing HO-1 expression in the aorta might be a promising therapeutic strategy for AAA

cardiology

International Academy of Cardiology Annual Scientific Sessions 2016 21st World Congress on Heart Disease, Boston, Mass., USA, July 30-August 1, 2016: Abstracts