Sponge‐induced angiogenesis and inflammation in PAF receptor‐deficient mice (PAFR‐KO)

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). Angiogenesis as...

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Published inBritish journal of pharmacology Vol. 141; no. 7; pp. 1185 - 1192
Main Authors Ferreira, Mônica A N D, Barcelos, Lucíola S, Campos, Paula P, Vasconcelos, Anilton C, Teixeira, Mauro M, Andrade, Silvia P
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.04.2004
Nature Publishing
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Abstract 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). 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. 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. 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. British Journal of Pharmacology (2004) 141, 1185–1192. doi:10.1038/sj.bjp.0705731
AbstractList 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.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.
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). 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. 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. 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. British Journal of Pharmacology (2004) 141 , 1185–1192. doi: 10.1038/sj.bjp.0705731
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.
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). 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. 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. 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. British Journal of Pharmacology (2004) 141, 1185–1192. doi:10.1038/sj.bjp.0705731
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). 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. 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. 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.
Author Barcelos, Lucíola S
Teixeira, Mauro M
Vasconcelos, Anilton C
Campos, Paula P
Ferreira, Mônica A N D
Andrade, Silvia P
AuthorAffiliation 3 3 Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil
2 2 Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil
1 1 Departments of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil
AuthorAffiliation_xml – name: 1 1 Departments of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil
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  givenname: Mônica A N D
  surname: Ferreira
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  fullname: Barcelos, Lucíola S
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Issue 7
Keywords Implant
growth factors
Animal origin
Inflammation
chemokines
Platelet-activating factor receptor
Chemokine
Marine environment
Angiogenesis
Porifera
Knockout mouse
sponge implants
Neovascularization
Invertebrata
Growth factor
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Snippet To determine biological functions of platelet‐activating factor (PAF) in chronic inflammation, we have investigated the kinetics of angiogenesis, inflammatory...
1. To determine biological functions of platelet-activating factor (PAF) in chronic inflammation, we have investigated the kinetics of angiogenesis,...
To determine biological functions of platelet-activating factor (PAF) in chronic inflammation, we have investigated the kinetics of angiogenesis, inflammatory...
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SubjectTerms Acetylglucosaminidase
Administration, Topical
Animals
Biological and medical sciences
Blood Vessels - growth & development
Blood Vessels - pathology
chemokines
Chemokines - metabolism
Dihydropyridines - adverse effects
Dihydropyridines - therapeutic use
Fibroblasts - pathology
Granulation Tissue - physiopathology
Granuloma - chemically induced
Granuloma - pathology
growth factors
Hemoglobins - chemistry
Imidazoles - adverse effects
Imidazoles - therapeutic use
Implants, Experimental - adverse effects
Inflammation - chemically induced
Inflammation - physiopathology
Inflammation - prevention & control
Macrophages - pathology
Medical sciences
Mice
Mice, Inbred BALB C
Mice, Knockout
Neovascularization
Neovascularization, Pathologic - chemically induced
Neovascularization, Pathologic - physiopathology
Neovascularization, Pathologic - prevention & control
Neutrophils - pathology
Peroxidase
Pharmacology. Drug treatments
Platelet Activating Factor - administration & dosage
Platelet Activating Factor - metabolism
Platelet Activating Factor - pharmacokinetics
Platelet Membrane Glycoproteins - antagonists & inhibitors
Platelet Membrane Glycoproteins - deficiency
Platelet Membrane Glycoproteins - genetics
Polyurethanes - administration & dosage
Polyurethanes - adverse effects
Polyurethanes - chemistry
Porifera - chemistry
Receptors, G-Protein-Coupled - antagonists & inhibitors
Receptors, G-Protein-Coupled - deficiency
Receptors, G-Protein-Coupled - genetics
Skin - blood supply
Skin - pathology
sponge implants
Title Sponge‐induced angiogenesis and inflammation in PAF receptor‐deficient mice (PAFR‐KO)
URI https://onlinelibrary.wiley.com/doi/abs/10.1038%2Fsj.bjp.0705731
https://www.ncbi.nlm.nih.gov/pubmed/15023865
https://www.proquest.com/docview/217193242
https://www.proquest.com/docview/71799129
https://pubmed.ncbi.nlm.nih.gov/PMC1574894
Volume 141
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