Targeting Robo4-Dependent Slit Signaling to Survive the Cytokine Storm in Sepsis and Influenza

by Nyall R. London, Weiquan Zhu, Fernando A. Bozza, Matthew C. P. Smith, Daniel M. Greif, Lise K. Sorensen, Luming Chen, Yuuki Kaminoh, Aubrey C. Chan, Samuel F. Passi, Craig W. Day, Dale L. Barnard, Guy A. Zimmerman, Mark A. Krasnow, and

Dean Y. Li

Sci Transl MedVolume 2(23):23ra19-23ra19

March 17, 2010

Published by AAAS

Fig. 1 Slit2N stabilizes the endothelium in vitro by enhancing VE-cadherin localization at the cell surface.

Nyall R. London et al., Sci Transl Med 2010;2:23ra19

Published by AAAS

Fig. 2 Slit2N enhances a VE-cadherin–p120-catenin interaction in vitro.

Nyall R. London et al., Sci Transl Med 2010;2:23ra19

Published by AAAS

Fig. 3 Slit2N inhibits LPS-induced permeability, protein exudates, and cell infiltrates in vivo.

Nyall R. London et al., Sci Transl Med 2010;2:23ra19

Published by AAAS

Fig. 4 Slit2N reduces permeability and mortality in a CLP model of sepsis.

Nyall R. London et al., Sci Transl Med 2010;2:23ra19

Published by AAAS

Fig. 5 Slit2N reduces mortality in models of H5N1 infection.

Nyall R. London et al., Sci Transl Med 2010;2:23ra19

Published by AAAS

Fig. 6 Slit reduces vascular leak caused by multiple inflammatory stimuli through enhancing VE-cadherin at the cell surface.

Nyall R. London et al., Sci Transl Med 2010;2:23ra19

Published by AAAS