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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:e137.)
© 2004 American Heart Association, Inc.

Letters to the Editor

TGF-ß in Atherosclerosis

Göran K. Hansson; Anna-Karin L. Robertson

Department of Medicine, Karolinska Institute, Stockholm, Sweden

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

In his excellent review on the role of transforming growth factor (TGF)-ß in atherosclerosis in the March 2004 issue of Arteriosclerosis, Thrombosis, and Vascular Biology,¹ David J. Grainger discusses the multiple roles of this growth factor and suggests that direct effects on vascular cells as well as effects exerted primarily on immune cells may account for its antiatherogenic properties. He points out the discrepancy between the experiments applying generalized TGF-ß suppression and those using dominant-negative (dn) TGF-ß receptors in T cells. Using neutralizing anti–TGF-ß antibodies in apoE–/– mice, Mallat et al observed an increased lesion size,² whereas transplantation of bone marrow containing T cells with dn–TGF-ß receptors led to reduced lesions.³ Therefore, Dr. Grainger concludes that TGF-ß signaling in the inflammatory cell population cannot be the whole story, and he suggests that the effects of this cytokine on smooth muscle cells (SMCs) determine the formation of matrix-rich, stable plaques. However, new data published after the acceptance of his review article suggests that immunosuppressive effects of TGF-ß modulate the growth and stability of the atherosclerotic lesion as well as its inflammatory properties.

In an article published in the November 2003 issue of the Journal of Clinical Investigation, we show that apoE–/– mice with abrogated TGF-ß signaling in T cells develop dramatically accelerated atherosclerosis with a several-fold increase in lesion size as well as a more vulnerable lesion phenotype with reduced collagen and increased inflammation.⁴ These proatherogenic effects were entirely caused by the lack of functional TGF-ß . . . [Full Text of this Article]

David J. Grainger

Department of Medicine, Cambridge University, Cambridge, England

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