title: Sponge-induced angiogenesis and inflammation in PAF receptor-deficient mice (PAFR-KO).
abstract: 1. To determine biological functions of platelet-activating factor (PAF) in chronic inflammation, we have investigated the kinetics of angiogenesis, inflammatory cells recruitment and cytokine production in sponge-induced granuloma in wild type and PAF receptor-deficient mice (PAFR-KO). 2. Angiogenesis as determined by morphometric analysis and hemoglobin content was significantly higher in the implants of PAFR-KO mice at all time points. Treatment with PAF receptor antagonist UK74505 (30 mg kg(-1)) also increased angiogenesis in sponge implants. 3. Neutrophils and macrophages accumulation, as determined by myeloperoxidase and N-acetylglucosaminidase activities in the supernatant of implanted sponges were markedly decreased in PAFR-KO mice. Surprisingly, the levels of the proinflammatory chemokines, keratinocyte-derived chemokine and chemokine monocyte chemoattractant protein 1 were higher in the implants of the transgenic animals. 4. We have shown that angiogenesis was stimulated in PAFR-KO mice whereas inflammation was decreased, indicating that PAF is an endogenous regulator of new blood vessels formation in the inflammatory microenvironment induced by the sponge implant.
authors.affiliation: Department of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil.
authors.forename: Mônica A N D
authors.initials: MA
authors.lastname: Ferreira
authors.forename: Lucíola S
authors.initials: LS
authors.lastname: Barcelos
authors.forename: Paula P
authors.initials: PP
authors.lastname: Campos
authors.forename: Anilton C
authors.initials: AC
authors.lastname: Vasconcelos
authors.forename: Mauro M
authors.initials: MM
authors.lastname: Teixeira
authors.forename: Silvia P
authors.initials: SP
authors.lastname: Andrade
mesh_terms: D000118:Acetylglucosaminidase; D000287:Administration, Topical; D000818:Animals; D001808:Blood Vessels / Q000254:growth & development / Q000473:pathology; D018925:Chemokines / Q000378:metabolism; D004095:Dihydropyridines / Q000009:adverse effects / Q000627:therapeutic use; D005347:Fibroblasts / Q000473:pathology; D006097:Granulation Tissue / Q000503:physiopathology; D006099:Granuloma / Q000139:chemically induced / Q000473:pathology; D006454:Hemoglobins / Q000737:chemistry; D007093:Imidazoles / Q000009:adverse effects / Q000627:therapeutic use; D020007:Implants, Experimental / Q000009:adverse effects; D007249:Inflammation / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control; D008264:Macrophages / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009389:Neovascularization, Pathologic / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control; D009504:Neutrophils / Q000473:pathology; D009195:Peroxidase; D010972:Platelet Activating Factor / Q000008:administration & dosage / Q000378:metabolism / Q000493:pharmacokinetics; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000172:deficiency* / Q000235:genetics*; D011140:Polyurethanes / Q000008:administration & dosage / Q000009:adverse effects* / Q000737:chemistry*; D011161:Porifera / Q000737:chemistry*; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000172:deficiency* / Q000235:genetics*; D012867:Skin / Q000098:blood supply / Q000473:pathology
chemical_list: D018925:Chemokines; D004095:Dihydropyridines; D006454:Hemoglobins; D007093:Imidazoles; D010972:Platelet Activating Factor; D010980:Platelet Membrane Glycoproteins; D011140:Polyurethanes; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; C115016:polyetherurethane; C073027:modipafant; D009195:Peroxidase; D000118:Acetylglucosaminidase