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Institute for Molecular & Cellular Regulation (K.M., A.M., Y.H., I.K.), Gunma University; and Department of Ophthalmology (K.M., S.K.); and Third Department of Internal Medicine (A.M.), Gunma University School of Medicine, Maebashi 371-8512, Japan
Address all correspondence and requests for reprints to: Itaru Kojima, M.D., Institute for Molecular & Cellular Regulation, Gunma University, Maebashi 371-8512, Japan. E-mail: ikojima{at}showa.gunma-u.ac.jp.
The present study was conducted to elucidate the role of activin A in tubulogenesis of vascular endothelial cells. Activin A was produced in bovine aortic endothelial cells (BAEC). These cells also expressed the type I and type II activin receptors. When added to BAEC cultured in a collagen gel, activin A induced capillary formation. Activin A was as potent as vascular endothelial growth factor (VEGF) and markedly enhanced VEGF-induced tubulogenesis. To examine the role of endogenous activin A, we added follistatin, an inhibitor of activin A. Follistatin nearly completely blocked the VEGF-induced tubulogenesis, and the effect of follistatin was reproduced by transfection of the dominant-negative type II activin receptor gene. In BAEC, activin A increased the expression of VEGF and the VEGF receptors, Flt-1 and Flk-1. On the other hand, VEGF increased the production of activin A. Finally, addition of follistatin, which blocks the action of endogenous activin A, reduced the expression of Flt-1 and Flk-1. These results indicate that an autocrine factor activin A amplifies the effect of VEGF by up-regulating VEGF and its receptors. This effect of activin A is critical in the VEGF-induced tubulogenic morphogenesis in BAEC.
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