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Patients with Gorham-Stout disease (GSD) have lymphatic vessels in their bones and their bones gradually disappear. Here, we report that mice that overexpress VEGF-C in bone exhibit a phenotype that resembles GSD. To drive VEGF-C expression in bone, we generated  Osx-tTA;TetO-Vegfc  double-transgenic mice. In contrast to  Osx-tTA  mice,  Osx-tTA;TetO-Vegfc  mice developed lymphatics in their bones. We found that inhibition of VEGFR3, but not VEGFR2, prevented the formation of bone lymphatics in  Osx-tTA;TetO-Vegfc  mice. Radiological and histological analysis revealed that bones from  Osx-tTA;TetO-Vegfc  mice were more porous and had more osteoclasts than bones from  Osx-tTA  mice. Importantly, we found that bone loss in  Osx-tTA;TetO-Vegfc  mice could be attenuated by an osteoclast inhibitor. We also discovered that the mutant phenotype of  Osx-tTA;TetO-Vegfc  mice could be reversed by inhibiting the expression of VEGF-C. Taken together, our results indicate that expression of VEGF-C in bone is sufficient to induce the pathologic hallmarks of GSD in mice.

VEGF-C promotes the development of lymphatics in bone and bone loss