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Induction of decay accelerating factor and membrane cofactor protein by resveratrol attenuates complement deposition

Maria G Detsika1, Eleni D Myrtsi2, Sofia D Koulocheri2

  • 1First Department of Critical Care Medicine and Pulmonary Services, Thorax Foundation, Research Center of Intensive Care and Emergency Thoracic Medicine, Evangelismos Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.

Biochemistry and Biophysics Reports
|June 14, 2019
PubMed

Insights

Resveratrol, found in red wine, protects against cardiovascular disease by boosting heme-oxygenase (HO)-1. This increases complement regulatory proteins, reducing harmful C3b deposition in blood vessels.

Area of Science:

  • Cardiovascular Disease Research
  • Immunology and Complement System
  • Molecular Biology and Cell Signaling

Background:

  • Complement activation is implicated in cardiovascular disease (CVD) progression and treatment.
  • Resveratrol, a compound in red wine, shows protective effects against CVD, but its mechanisms are unclear.
  • Understanding resveratrol's molecular targets is crucial for developing targeted CVD therapies.

Purpose of the Study:

  • To investigate if resveratrol's CVD protective effects are mediated by upregulating complement regulatory proteins via heme-oxygenase (HO)-1 induction.
  • To assess resveratrol's impact on HO-1, membrane cofactor protein (MCP, CD46), decay-accelerating factor (DAF, CD55), and CD59 expression in human coronary artery endothelial cells (HCAECs).
  • To determine the role of HO-1 and DAF in resveratrol's ability to reduce complement-mediated C3b deposition.

Main Methods:

  • HCAECs were treated with resveratrol at concentrations found in red wine.
  • HO-1, MCP (CD46), DAF (CD55), and CD59 expression levels were measured.
  • HO-1 was silenced using siRNAs, and DAF function was blocked with an antibody.
  • C3b deposition was quantified after complement activation using normal human or rat serum.

Main Results:

  • Resveratrol significantly increased HO-1, MCP (CD46), and DAF (CD55) expression in HCAECs, with no effect on CD59.
  • Silencing HO-1 abolished resveratrol-induced MCP and DAF expression.
  • Resveratrol-induced MCP and DAF reduced C3b deposition.
  • Blocking DAF or silencing HO-1 increased C3b deposition in the presence of complement.

Conclusions:

  • Resveratrol protects against cardiovascular disease through a novel mechanism involving HO-1 induction.
  • HO-1 upregulates complement regulatory proteins DAF and MCP, which reduce harmful C3b deposition.
  • This study highlights the critical role of the HO-1/DAF pathway in mediating resveratrol's cardioprotective effects.

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