Angiogenesis is a multi-step process that involves the activation, proliferation, and migration of endothelial cells. We have recently shown that TGF-${eta}1$ can induce mouse macrophages to produce VEGF, a potent angiogenic factor. In the present study, we explored whether TGF-${eta}1$ has a similar effect on mouse dendritic cells. First, we show that under hypoxic conditions, TGF-${eta}1$ induced the expression of VEGF transcripts in bone marrow-derived dendritic cells. Overexpression of Smad3/4 further augmented TGF-${eta}1$-induced VEGF transcription, while overexpression of DN-Smad3 decreased VEGF transcription in DC2.4 cells, a mouse dendritic cell line. We also show that TGF-${eta}1$ and Smads are involved in the induction of VEGF protein secretion. Interestingly, under the same conditions, the expression of VEGF receptor 1 (Flt-1) was also elevated at both the transcriptional and protein levels. Additionally, we found that the TGF-${eta}1$-induced VEGF secretion in activated DC2.4 cells has wound-healing properties. Finally, Smad7 and Smurf1 negatively regulated the TGF-${eta}1$-induced and Smad3/4-mediated VEGF expression. Taken together, these results indicate that TGF-${eta}1$ can enhance the expression of VEGF and Flt-1 through the typical Smad pathway in mouse dendritic cells.