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Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells.

Publication ,  Journal Article
Zhang, L; Peppel, K; Brian, L; Chien, L; Freedman, NJ
Published in: Arterioscler Thromb Vasc Biol
December 2004

OBJECTIVE: Vein graft remodeling and neointimal hyperplasia involve inflammation, graft-intrinsic cells, and recruitment of vascular progenitor cells. We sought to examine if the inflammatory cytokine tumor necrosis factor (TNF) affects vein graft remodeling via its p55 TNF receptor-1 (p55). METHODS AND RESULTS: Inferior vena cava-to-carotid artery interposition grafting was performed between p55-/- and congenic (C57Bl/6) wild-type (WT) mice. Immunofluorescence revealed TNF in early (2-week) vein grafts. Six weeks postoperatively, luminal and medial areas were indistinguishable among all vein graft groups. However, neointimal area was reduced in p55-/- grafts: by 40% in p55-/- grafts placed in p55-/- recipients, and by 21% in p55-/- grafts placed in WT recipients, compared with WT grafts in WT recipients (P<0.05). In 2-week-old vein grafts, p55 deficiency reduced intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1 expression by 50% to 60%, and increased the extent of graft endothelialization. In vitro, TNF promoted chemokine expression and [3H]thymidine incorporation in vascular smooth muscle cells (SMCs) from WT, but not from p55-/- mice. However, responses of WT and p55-/- SMCs to other growth factors were equivalent. CONCLUSIONS: Signaling via p55, in vein graft-intrinsic cells, contributes to the pathogenesis of vein graft neointimal hyperplasia.

Duke Scholars

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Published In

Arterioscler Thromb Vasc Biol

DOI

EISSN

1524-4636

Publication Date

December 2004

Volume

24

Issue

12

Start / End Page

2277 / 2283

Location

United States

Related Subject Headings

  • Vena Cava, Inferior
  • Veins
  • Tunica Intima
  • Tumor Necrosis Factor-alpha
  • Signal Transduction
  • Receptors, Tumor Necrosis Factor, Type I
  • Neovascularization, Pathologic
  • Mice, Inbred C57BL
  • Mice, Congenic
  • Mice
 

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Zhang, L., Peppel, K., Brian, L., Chien, L., & Freedman, N. J. (2004). Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells. Arterioscler Thromb Vasc Biol, 24(12), 2277–2283. https://doi.org/10.1161/01.ATV.0000147766.68987.0d
Zhang, Lisheng, Karsten Peppel, Leigh Brian, Lynn Chien, and Neil J. Freedman. “Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells.Arterioscler Thromb Vasc Biol 24, no. 12 (December 2004): 2277–83. https://doi.org/10.1161/01.ATV.0000147766.68987.0d.
Zhang L, Peppel K, Brian L, Chien L, Freedman NJ. Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells. Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):2277–83.
Zhang, Lisheng, et al. “Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells.Arterioscler Thromb Vasc Biol, vol. 24, no. 12, Dec. 2004, pp. 2277–83. Pubmed, doi:10.1161/01.ATV.0000147766.68987.0d.
Zhang L, Peppel K, Brian L, Chien L, Freedman NJ. Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells. Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):2277–2283.

Published In

Arterioscler Thromb Vasc Biol

DOI

EISSN

1524-4636

Publication Date

December 2004

Volume

24

Issue

12

Start / End Page

2277 / 2283

Location

United States

Related Subject Headings

  • Vena Cava, Inferior
  • Veins
  • Tunica Intima
  • Tumor Necrosis Factor-alpha
  • Signal Transduction
  • Receptors, Tumor Necrosis Factor, Type I
  • Neovascularization, Pathologic
  • Mice, Inbred C57BL
  • Mice, Congenic
  • Mice