The release of nitric oxide from S-nitrosothiols promotes angiogenesis

PLoS One. 2006 Dec 20;1(1):e25. doi: 10.1371/journal.pone.0000025.

Abstract

Background: Free nitric oxide (NO) reacts with sulphydryl residues to form S-nitrosothiols, which act as NO reservoirs. We sought to determine whether thiol-preserving agents and antioxidants, such as dithiothreitol (DTT) and vitamin C, induce NO release from S-nitrosylated proteins in endothelial cell cultures to promote angiogenesis.

Methodology/principal findings: NO release was measured directly in cell supernatants using a Sievers NO Analyser, and in vitro angiogenesis was assessed by quantifying capillary-like tube network formation of porcine aortic endothelial cells (PAEC) on growth factor-reduced Matrigel. Incubation of PAEC with DTT or vitamin C significantly increased NO release in a concentration-dependent manner. However, the nitric oxide synthase (NOS) inhibitors, L-NNA and L-NIO, had no effect on DTT- or vitamin C-induced NO release, and there was no concomitant increase in the phosphorylation of endothelial NOS at serine-1177 following DTT or vitamin C treatment. DTT and vitamin C increased capillary-like tube network formation by nine- and two-fold, respectively, and the addition of copper ions doubled the effect of vitamin C. Surprisingly, DTT maintained endothelial tube networks for up to one month under serum-free conditions, and selective inhibitors of guanylyl cyclase (ODQ) and PKG (KT-5823) blocked this, demonstrating the requirement of cyclic GMP and PKG in this process.

Conclusions/significance: Both DTT and vitamin C are capable of releasing sufficient NO from S-nitrosothiols to induce capillary morphogenesis. This study provides the first evidence that increased denitrosylation leads to increased bioavailability of NO, independent of NOS activity, to promote sustained angiogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascorbic Acid / pharmacology
  • Carbazoles / pharmacology
  • Cells, Cultured
  • Culture Media, Serum-Free
  • Cyclic GMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic GMP-Dependent Protein Kinases / metabolism
  • Dithiothreitol / pharmacology
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Enzyme Inhibitors / pharmacology
  • Guanylate Cyclase / antagonists & inhibitors
  • Guanylate Cyclase / metabolism
  • Neovascularization, Physiologic* / drug effects
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type III / antagonists & inhibitors
  • Nitric Oxide Synthase Type III / chemistry
  • Nitric Oxide Synthase Type III / metabolism
  • Nitroarginine / pharmacology
  • Ornithine / analogs & derivatives
  • Ornithine / pharmacology
  • Oxadiazoles / pharmacology
  • Phosphorylation
  • Quinoxalines / pharmacology
  • S-Nitrosothiols / metabolism*
  • Swine

Substances

  • 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one
  • Carbazoles
  • Culture Media, Serum-Free
  • Enzyme Inhibitors
  • Oxadiazoles
  • Quinoxalines
  • S-Nitrosothiols
  • KT 5823
  • Nitroarginine
  • Nitric Oxide
  • N(G)-iminoethylornithine
  • Ornithine
  • Nitric Oxide Synthase Type III
  • Cyclic GMP-Dependent Protein Kinases
  • Guanylate Cyclase
  • Ascorbic Acid
  • Dithiothreitol