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Published online before print May 13, 2005

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1104682

Received for publication November 22, 2004.
Revised April 5, 2005.
Accepted for publication April 6, 2005.

Article

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

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

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

^@ To whom correspondence should be addressed. E-mail: mmtex{at}icb.ufmg.br.

	Abstract

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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