title: Impaired inflammatory angiogenesis, but not leukocyte influx, in mice lacking TNFR1.
abstract: The majority of biological responses classically attributed to tumor necrosis factor alpha (TNF-alpha) 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.
authors.affiliation: Department of Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos, 6627-Pampulha, 31270-901 Belo Horizonte, MG, Brazil.
authors.forename: L S
authors.initials: LS
authors.lastname: Barcelos
authors.forename: A
authors.initials: A
authors.lastname: Talvani
authors.forename: A S
authors.initials: AS
authors.lastname: Teixeira
authors.forename: L Q
authors.initials: LQ
authors.lastname: Vieira
authors.forename: G D
authors.initials: GD
authors.lastname: Cassali
authors.forename: S P
authors.initials: SP
authors.lastname: Andrade
authors.forename: M M
authors.initials: MM
authors.lastname: Teixeira
mesh_terms: D000118:Acetylglucosaminidase / Q000032:analysis; D000818:Animals; D018925:Chemokines / Q000378:metabolism; D005260:Female; D006454:Hemoglobins / Q000032:analysis; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009389:Neovascularization, Pathologic / Q000378:metabolism*; D020556:Neutrophil Infiltration / Q000235:genetics; D009195:Peroxidase / Q000032:analysis; D011091:Polyesters; D011140:Polyurethanes; D019736:Prostheses and Implants; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018925:Chemokines; D006454:Hemoglobins; D011091:Polyesters; D011140:Polyurethanes; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D000118:Acetylglucosaminidase