Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice

Barcelos, L.S., Coelho, A.M., Russo, R.C., Guabiraba Brito, R., Souza, A.L.S., Bruno-Lima Jr., G., Proudfoot, A.E.I., Andrade, S.P. and Teixeira, M.M. (2009) Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice. Microvascular Research, 78(2), pp. 148-154. (doi:10.1016/j.mvr.2009.04.009)

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Publisher's URL: http://dx.doi.org/10.1016/j.mvr.2009.04.009

Abstract

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.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Guabiraba Brito, Dr Rodrigo
Authors: Barcelos, L.S., Coelho, A.M., Russo, R.C., Guabiraba Brito, R., Souza, A.L.S., Bruno-Lima Jr., G., Proudfoot, A.E.I., Andrade, S.P., and Teixeira, M.M.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Microvascular Research
ISSN:0026-2862

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