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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 297/3/L420    most recent 90477.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Takagi, Y. Articles by Hasegawa, Y. PubMed PubMed Citation Articles by Takagi, Y. Articles by Hasegawa, Y.

Erythromycin-induced CXCR4 expression on microvascular endothelial cells

¹Department of Respiratory Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan; ²Department of Pathology, University of Michigan, Ann Arbor, Michigan; ³Department of Medical Technology, Nagoya University Graduate School of Health Science, Nagoya, Japan; and ⁴College of Life and Health Sciences, Department of Biomedical Sciences, Chubu University, Kasugai, Japan

Submitted 8 September 2008 ; accepted in final form 3 June 2009

Although stromal-derived factor-1 (SDF-1) via its cognate receptor CXCR4 is assumed to play a critical role in migration of endothelial cells during new vessel formation after tissue injury, CXCR4 expression on endothelial cells is strictly regulated. Erythromycin (EM), a 14-membered ring macrolide, has an anti-inflammatory effect that may account for its clinical benefit in the treatment of chronic inflammatory diseases. However, the effects of EM on endothelial cells and especially their expression of CXCR4 have not been fully evaluated. In this study, we demonstrated that EM markedly induced CXCR4 surface expression on microvascular endothelial cells in vitro and lung capillary endothelial cells in vivo. This ability to induce CXCR4 surface expression on endothelial cells was restricted to 14-membered ring macrolides and was not observed in other antibiotics including a 16-membered ring macrolide, josamycin. Furthermore, this EM-induced expression of CXCR4 on endothelial cells was functionally significant as demonstrated by chemotaxis assays in vitro. These findings suggest that EM-induced CXCR4 surface expression on endothelial cells may promote migration of CXCR4-expressing endothelial cells into sites of tissue injury, which may be associated with the known anti-inflammatory activity of this macrolide.

stromal-derived factor-1; angiogenesis