期刊
BLOOD
卷 118, 期 18, 页码 5050-5059出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2011-03-343293
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资金
- German Research Council [C1, A2, 834]
- Excellence Cluster Cardiopulmonary Systems
In human inflammatory diseases, we identified endothelial angiopoietin-2 (Ang-2) expression to be strongly associated with inflammations mediated by myeloid cells but not lymphocytes. To identify the underlying mechanism, we made use of a transgenic mouse model with inducible endothelial cell-specific expression of Ang-2. In this model, in the absence of inflammatory stimuli, long-term expression of Ang-2 led to a time-dependent accumulation of myeloid cells in numerous organs, suggesting that Ang-2 is sufficient to recruit myeloid cells. In models of acute inflammation, such as delayed-type hypersensitivity and peritonitis, Ang-2 transgenic animals showed an increased responsiveness. Intravital fluorescence video microscopy revealed augmented cell adhesion as an underlying event. Consequently, we demonstrated that Ang-2 is able to induce strong monocyte adhesion under shear in vitro, which could be blocked by antibodies to beta(2)-integrin. Taken together, our results describe Ang-2 as a novel, endothelialderived regulator of myeloid cell infiltration that modulates beta(2)-integrin-mediated adhesion in a paracrine manner. (Blood. 2011; 118(18):5050-5059)
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