趋化因子CXCL1-3/KC和CCL2/JE在小鼠炎症性血管生成模型中的产生及体内效应

Production and in vivo effects of chemokines CXCL1-3/KC and CCL2/JE in a model of inflammatory angiogenesis in mice.

作者信息

Barcelos L S, Talvani A, Teixeira A S, Cassali G D, Andrade S P, Teixeira M M

机构信息

Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos, 6627-Pampulha, 31270-901, Belo Horizonte MG, Brasil.

出版信息

Inflamm Res. 2004 Oct;53(10):576-84. doi: 10.1007/s00011-004-1299-4.

DOI:10.1007/s00011-004-1299-4

PMID:15597153

Abstract

OBJECTIVE

Using the murine sponge model, we investigated the temporal relationship between angiogenesis, leukocyte accumulation and endogenous generation of the pro-inflammatory chemokines CXCL1-3/KC and CCL2/JE. Furthermore, the effects of exogenous administration of these chemokines were studied.

METHODS

Angiogenesis in the implants was assessed by measuring the hemoglobin content (vascular index) and leukocyte accumulation quantified by evaluating MPO and NAG enzyme activities.

RESULTS

A progressive increase in hemoglobin content and in enzymatic activities was observed during the whole period. The levels of CXCL1-3/KC and CCL2/JE in the implants peaked at days 7 and 1, respectively. Exogenous administration of CXCL1-3/KC (100 ng/day intra-implant) applied at days 1-3 resulted in increased neovascularization and macrophage accumulation. Intra-implant injections of CCL2/JE (100 ng/day) also resulted in increased angiogenesis and macrophage accumulation.

CONCLUSIONS

These results demonstrated that the chemokines, CXCL1-3/KC and CCL2/JE, are generated within the sponge compartment and that neovascularization and inflammatory cells influx can be modulated by exogenous administration of the chemokines.

摘要

目的

利用小鼠海绵模型，我们研究了血管生成、白细胞聚集与促炎趋化因子CXCL1 - 3/KC和CCL2/JE内源性生成之间的时间关系。此外，还研究了外源性给予这些趋化因子的作用。

方法

通过测量血红蛋白含量（血管指数）评估植入物中的血管生成，并通过评估MPO和NAG酶活性对白细胞聚集进行定量。

结果

在整个期间观察到血红蛋白含量和酶活性逐渐增加。植入物中CXCL1 - 3/KC和CCL2/JE的水平分别在第7天和第1天达到峰值。在第1 - 3天给予外源性CXCL1 - 3/KC（100 ng/天，植入物内）导致新血管形成增加和巨噬细胞聚集。植入物内注射CCL2/JE（100 ng/天）也导致血管生成增加和巨噬细胞聚集。