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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4321-4329.
Prepublished online as a Blood First Edition Paper on January 4, 2005; DOI 10.1182/blood-2004-07-2885.
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Submitted July 27, 2004
Accepted December 16, 2004
Sema4D induces angiogenesis through Met recruitment by Plexin B1
Paolo Conrotto, Donatella Valdembri, Simona Corso, Guido Serini, Luca Tamagnone, Paolo M Comoglio, Federico Bussolino, and Silvia Giordano*
Division of Molecular Oncology, IRCC, Institute for Cancer Research and Treatment, University of Torino School of Medicine, Candiolo, Torino, Italy
Division of Experimental Angiogenesis, IRCC, Institute for Cancer Research and Treatment, University of Torino School of Medicine, Candiolo, Torino, Italy
* Corresponding author; email: silvia.giordano{at}ircc.it.
Semaphorins, a large family of membrane-bound and secreted proteins, signal through their transmembrane receptors, the plexins. Both semaphorins and plexins share structural homologies with scatter factor receptors, a family of tyrosine kinase receptors for which Met is the prototype. Semaphorins have been mostly studied in the developing nervous system, where they act as repelling cues in axon guidance. However, they are widely expressed in several tissues and their role in epithelial morphogenesis has been recently established. Not much is known on their role in angiogenesis, a key step during both embryonic development and adulthood. Here we demonstrate that a semaphorin, Sema4D, is angiogenic both in vitro and in vivo and that this effect is mediated by its high affinity receptor, PlexinB1. Moreover, we also prove that biological effects elicited by PlexinB1 require coupling and activation of the Met tyrosine kinase. In sum, we identify for the first time a pro-angiogenic semaphorin and provide insight on the signaling machinery exploited by PlexinB1 to control angiogenesis.
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