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Related Experiment Video

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Physiological levels of thrombospondin-1 decrease NO-dependent vasodilation in coronary microvessels from aged rats.

Chris Nevitt1, Grant McKenzie2, Katelyn Christian2

  • 1Cardiovascular Innovation Institute, University of Louisville, Louisville, Kentucky; Department of Biochemistry and Molecular Genetics, University of Louisville, Louisville, Kentucky; and.

American Journal of Physiology. Heart and Circulatory Physiology
|May 21, 2016
PubMed
Summary

Blocking CD47 improves nitric oxide (NO) signaling in aged coronary arterioles, restoring blood flow and potentially reversing age-related cardiovascular dysfunction. This finding offers a new therapeutic target for improving heart health in older individuals.

Keywords:
CD47agingcoronary blood flownitric oxidethrombospondin-1

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Area of Science:

  • Cardiovascular Physiology
  • Aging Research
  • Vascular Biology

Background:

  • Aging diminishes nitric oxide (NO) signaling, impairing coronary blood flow reserve (CFR).
  • Thrombospondin-1 (Thbs-1) limits NO-dependent vasodilation via CD47 and superoxide (O2(-)) formation, particularly in peripheral vessels.

Purpose of the Study:

  • To test if blocking CD47 improves NO-mediated vasoreactivity and CFR in aged coronary arterioles.
  • To investigate the role of Thbs-1 and CD47 in age-related coronary microvascular dysfunction.

Main Methods:

  • Isolated coronary arterioles from young and old rats were exposed to NO donors and Thbs-1/CD47 blocking antibodies.
  • Vessel relaxation and O2(-) production were measured.
  • In vivo CFR was assessed in aged rats following CD47 antibody treatment.

Main Results:

  • Thbs-1 inhibited NO-mediated vasodilation and increased O2(-) production in aged arterioles, an effect exaggerated with aging.
  • CD47 blocking antibody restored NO-dependent vasodilation and reduced O2(-) in aged arterioles.
  • In vivo, αCD47 treatment significantly increased CFR in aged rats.

Conclusions:

  • The impact of Thbs-1 and CD47 on coronary perfusion is amplified with aging.
  • Targeting CD47 may reverse age-related coronary microvascular dysfunction.
  • CD47 blockade represents a potential therapeutic strategy for cardiovascular health in aging.