Inhibitory effects of calcitonin gene-related peptides on experimental vein graft disease

Ann Thorac Surg. 2010 Jul;90(1):117-23. doi: 10.1016/j.athoracsur.2010.03.063.

Abstract

Background: Vein graft disease is a chronic inflammatory disease and limits the long-term clinical outcome of coronary revascularization. Because calcitonin gene-related peptide (CGRP) inhibits macrophage infiltration and inflammatory mediators, we hypothesized that transfected CGRP gene would inhibit macrophage infiltration and expression of inflammatory mediators in vein graft disease.

Methods: Autologous rabbit jugular vein grafts were incubated ex vivo in a solution of mosaic adeno-associated virus vectors containing CGRP gene (AAV2/1.CGRP) or Escherichia coli B-galactosidase gene (LacZ) or a saline solution and then interposed in the carotid artery. Expression of CGRP gene was identified by reverse transcription-polymerase chain reaction, and E. coli LacZ gene expression was identified by X-gal staining. Intima to media ratios were evaluated at postoperative 4 weeks. Macrophages were identified with CD68 antibody by immunocytochemistry. Inflammatory mediators were measured with real-time polymerase chain reaction.

Results: The CGRP and LacZ gene expression were positive at postoperative 4 weeks. The intima to media ratio was significantly inhibited in the AAV2/1.CGRP group. Macrophage infiltration and expression of inflammatory mediators including monocyte chemoattractant protein-1, tumor necrosis factor-alpha, inducible nitric oxide synthase, and matrix metalloproteinase-9 were also significantly inhibited in the AAV2/1.CGRP group.

Conclusions: Transfection of AAV2/1.CGRP inhibited inflammatory mediator expression, macrophage infiltration, and neointimal hyperplasia in experimental vein graft disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcitonin Gene-Related Peptide / genetics*
  • Chemokine CCL2 / biosynthesis
  • Coronary Artery Bypass / adverse effects*
  • Gene Expression
  • Genetic Vectors
  • Graft Occlusion, Vascular / genetics*
  • Graft Occlusion, Vascular / immunology*
  • Hyperplasia
  • Lac Operon
  • Macrophages / immunology*
  • Male
  • Matrix Metalloproteinase 9 / biosynthesis
  • Nitric Oxide Synthase Type II / biosynthesis
  • Rabbits
  • Transfection
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tunica Intima / immunology
  • Tunica Intima / pathology

Substances

  • Chemokine CCL2
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide Synthase Type II
  • Matrix Metalloproteinase 9
  • Calcitonin Gene-Related Peptide