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Sustained decrease in superoxide dismutase activity underlies constrictive remodeling after balloon injury in

Paulo F Leite1, Alexandre Danilovic, Patricia Moriel

  • 1Vascular Biology Laboratory, Heart Institute, University of São Paulo School of Medicine, Av. Enéas de Carvalho Aguiar, 44, subsolo, CEP 05403-000 São Paulo, Brazil.

Arteriosclerosis, Thrombosis, and Vascular Biology
|September 6, 2003
PubMed
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Low vascular superoxide dismutase (SOD) activity after injury promotes vascular remodeling and oxidative stress. Restoring extracellular SOD (ecSOD) activity mitigates these effects, highlighting SOD

Area of Science:

  • Vascular biology and pathophysiology
  • Redox signaling in cardiovascular disease
  • Biochemistry of enzymatic antioxidant defense

Background:

  • Vascular repair mechanisms following injury are not fully elucidated.
  • Oxidative and nitrative stress play critical roles in post-injury vascular remodeling.
  • The specific contribution of vascular superoxide dismutase (SOD) activity to these processes remains unclear.

Purpose of the Study:

  • To investigate the role of vascular SOD activity in oxidative/nitrative stress and vascular caliber loss after injury.
  • To determine the impact of extracellular SOD (ecSOD) administration on vascular repair markers.

Main Methods:

  • Rabbits underwent iliac artery balloon overdistension, with follow-up for 14 days.
  • Vascular SOD activity, protein expression, and immunoreactivity to nitrotyrosine and nitric oxide synthases (NOS) were assessed.

Related Experiment Videos

  • Administration of ecSOD was performed from days 7 to 14 post-injury.

    • Main Results:

    • Vascular SOD activity significantly decreased 7 and 14 days post-injury.
    • Extracellular SOD (ecSOD) and CuZn SOD activities were reduced, while protein levels remained stable or increased.
    • Administration of ecSOD corrected SOD activity, reduced caliber loss by 59%, increased nitrate levels, and decreased nitrotyrosine and neuronal NOS expression.

    Conclusions:

    • Sustained low vascular SOD activity is crucial in promoting constrictive remodeling and oxidative stress post-injury.
    • Impaired SOD activity leads to reduced nitric oxide (NO) bioavailability from inducible NOS (iNOS).
    • SOD function critically influences the net outcome of iNOS induction in vivo, determining its beneficial or detrimental effects.