OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS: CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.
OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS:CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.
Authors: Rafael E Marques; Rodrigo Guabiraba; Juliana L Del Sarto; Rebeca F Rocha; Ana Luiza Queiroz; Daniel Cisalpino; Pedro E Marques; Carolina C Pacca; Caio T Fagundes; Gustavo B Menezes; Maurício L Nogueira; Danielle G Souza; Mauro M Teixeira Journal: Immunology Date: 2015-06-01 Impact factor: 7.397
Authors: Walter E Cromer; J Michael Mathis; Daniel N Granger; Ganta V Chaitanya; J Steven Alexander Journal: World J Gastroenterol Date: 2011-02-07 Impact factor: 5.742
Authors: Rodrigo Guabiraba; Remo C Russo; Amanda M Coelho; Mônica A N D Ferreira; Gabriel A O Lopes; Ariane K C Gomes; Silvia P Andrade; Luciola S Barcelos; Mauro M Teixeira Journal: Inflamm Res Date: 2013-05-31 Impact factor: 4.575
Authors: Carlos Eduardo Repeke; Samuel Barros Ferreira; Andreia Espindola Vieira; Elcia Maria Silveira; Mario Julio Avila-Campos; João Santana da Silva; Carlos Ferreira Santos; Ana Paula Campanelli; Ana Paula Favaro Trombone; Gustavo Pompermaier Garlet Journal: PLoS One Date: 2011-07-20 Impact factor: 3.240