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Published online before print May 13, 2005

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(Journal of Leukocyte Biology. 2005;78:352-358.)
© 2005 by Society for Leukocyte Biology

Impaired inflammatory angiogenesis, but not leukocyte influx, in mice lacking TNFR1

L. S. Barcelos^*, A. Talvani^*,1, A. S. Teixeira, L. Q. Vieira^*, G. D. Cassali, S. P. Andrade and M. M. Teixeira^*,2

^* Departments of Bioquímica e Imunologia,
Fisiologia e Biofísica, and
Patologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil

² Correspondence: Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos, 6627-Pampulha, 31270-901 Belo Horizonte, MG, Brazil. E-mail: mmtex{at}icb.ufmg.br

The majority of biological responses classically attributed to tumor necrosis factor (TNF-) is mediated by p55 receptor (TNFR1). Here, we aimed to clarify the biological role of TNFR1-mediated signals in an in vivo inflammatory angiogenesis model. Polyester-polyurethane sponges, used as a framework for tissue growth, were implanted in C57Bl/6 mice. These implants were collected at days 1, 7, and 14 post-implant for enzyme-linked immunosorbent assay or at days 7 and 14 for hemoglobin, myeloperoxidase, and N-acetylglucosaminidase measurements, used as indexes for angiogenesis, neutrophil, and macrophage accumulation, respectively. In TNFR1-deficient C57Bl/6 mice, there was a significant decrease in sponge vascularization but not in late inflammatory cell influx. It is interesting that levels of vascular endothelial growth factor were significantly lower in TNFR1-deficient than in wild-type mice at days 1 and 7. Levels of angiogenic chemokines, CC chemokine ligand 2/murine homologue of monocyte chemoattractant protein-1 and CXC chemokine ligand 1–3/keratinocyte-derived chemokine, were significantly lower in TNFR1-deficient mice at days 1 and 7 after implantation, respectively. These observations suggest that TNFR1-mediated signals have a critical role in sponge-induced angiogenesis, possibly by influencing the effector state of inflammatory cells and hence, modulating the angiogenic molecular network.

Key Words: TNF- • neutrophil • macrophage • p55 receptor

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