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Transforming Growth Factor-β: Role in Mediating Serum-Induced Endothelin Production by Vascular Endothelial Cells^*

Peptide Biology Laboratory (M. R. B., L. L. J.), Departments of Medicine and Surgery, University of California San Diego, La Jolla, California 92093-0817
Clayton Foundation Laboratories for Peptide Biology (J. V., W. V.), The Salk Institute for Biological Studies, La Jolla, California 92037; and The Whittier Institute (A. B), Scripps Memorial Hospital La Jolla, California 92037

Address all correspondence and requests for reprints to: Dr. Marvin R. Brown, Departments of Medicine and Surgery, 0817, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0817.

Abstract

Studies were performed to characterize the identity of the factors present in calf serum that stimulate endothelin (ET) production by vascular endothelial cells in culture. Two putative candidates responsible for the ET-releasing activity present in serum are members of the transforming growth factor-β (TGFβ) superfamily, TGFβ₁; and activin A. TGFβ₁ antiserum was used to block the actions of TGFβ₁, and follistatin was used to block the actions of activin. Treatment of serum with TGF5beta;₁ antiserum attenuates ET production by vascular endothelial cells. TGFβ₁ antiserum (1 µl) completely prevents the release of ET produced by 0.1% and 0.3% serum. Follistatin is a potent inhibitor of activin-induced ET release but does not alter seruminduced ET production. Because serum-induced ET release is dependent on TGFβ, it may be a physiological regulator of ET production by vascular endothelial cells. (Endocrinology 129: 2355–2360,1991)

Footnotes

^* This work was supported by NIH Grants HL-54154, NS-08671, AM-26741, and DH-26741, and by the San Diego Burn Institute.

Received May 17, 1991.

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