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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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Submitted October 25, 2007
Accepted February 23, 2008

Inhibition of endogenous TGF-{beta} signaling enhances lymphangiogenesis

Masako Oka, Caname Iwata, Hiroshi I Suzuki, Kunihiko Kiyono, Yasuyuki Morishita, Tetsuro Watabe, Akiyoshi Komuro, Mitsunobu R Kano, and Kohei Miyazono*

Department of Molecular Pathology, University of Tokyo, Tokyo, Japan

* Corresponding author; email: miyazono-ind{at}umin.ac.jp.

Lymphangiogenesis is induced by various growth factors, including VEGF-C. Although TGF-{beta} plays crucial roles in angiogenesis, the roles of TGF-{beta} signaling in lymphangiogenesis are unknown. We show here that TGF-{beta} transduced signals in human dermal lymphatic microvascular endothelial cells (HDLECs), and inhibited the proliferation, cord formation, and migration towards 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-{beta}, but were induced by TGF-{beta} type I receptor (T{beta}R-I) inhibitor. Moreover, inhibition of endogenous TGF-{beta} signaling by T{beta}R-I inhibitor accelerated lymphangiogenesis in a mouse model of chronic peritonitis. Lymphangiogenesis was also induced by T{beta}R-I inhibitor in the presence of VEGF-C in pancreatic adenocarcinoma xenograft models inoculated in nude mice. These findings suggest that TGF-{beta} transduces signals in LECs and plays an important role in the regulation of lymphangiogenesis in vivo.


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