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 Blood, 1 May 2008, Vol. 111, No. 9, pp. 4571-4579.
Prepublished online as a Blood First Edition Paper on February 29, 2008; DOI 10.1182/blood-2007-10-120337.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Inhibition of endogenous TGF-β signaling enhances lymphangiogenesis

Masako Oka1, Caname Iwata1, Hiroshi I. Suzuki1, Kunihiko Kiyono1, Yasuyuki Morishita1, Tetsuro Watabe1, Akiyoshi Komuro1, Mitsunobu R. Kano1, and Kohei Miyazono1

1 Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

Lymphangiogenesis is induced by various growth factors, including VEGF-C. Although TGF-β plays crucial roles in angiogenesis, the roles of TGF-β signaling in lymphangiogenesis are unknown. We show here that TGF-β transduced signals in human dermal lymphatic microvascular endothelial cells (HDLECs) and inhibited the proliferation, cord formation, and migration toward VEGF-C of HDLECs. Expression of lymphatic endothelial cell (LEC) markers, including LYVE-1 and Prox1 in HDLECs, as well as early lymph vessel development in mouse embryonic stem cells in the presence of VEGF-A and C, were repressed by TGF-β but were induced by TGF-β type I receptor (TβR-I) inhibitor. Moreover, inhibition of endogenous TGF-β signaling by TβR-I inhibitor accelerated lymphangiogenesis in a mouse model of chronic peritonitis. Lymphangiogenesis was also induced by TβR-I inhibitor in the presence of VEGF-C in pancreatic adenocarcinoma xenograft models inoculated in nude mice. These findings suggest that TGF-β transduces signals in LECs and plays an important role in the regulation of lymphangiogenesis in vivo.


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