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Integrative Physiology |
From the Institut National de la Santé et de la Recherche Médicale (Z.M., A.G., B.E., R.M., A.T.), INSERM U541, Institut Fédératif de Recherche "Circulation Paris 7," Hôpital Lariboisière; and ICGM-INSERM U477, Hôpital Cochin (C. M.-F., C.K., D.F.), Paris, France.
Correspondence to Ziad Mallat, MD, PhD, INSERM U541, Hôpital Lariboisière, 41 Bd de la chapelle, 75010 Paris, France. E-mail ziad.mallat{at}inserm.lrb.ap-hop-paris.fr
Abstract Atherosclerosis is a disease of the arterial wall that seems to be tightly modulated by the local inflammatory balance. Whereas a large body of evidence supports a role for proinflammatory mediators in disease progression, the understanding of the role of the antiinflammatory component in the modulation of plaque progression is only at its beginning. TGF-ß1, -ß2, and -ß3 are cytokines/growth factors with broad activities on cells and tissues in the cardiovascular system and have been proposed to play a role in the pathogenesis of atherosclerosis. However, no study has examined the direct role of TGF-ß in the development and composition of advanced atherosclerotic lesions. In the present study, we show that inhibition of TGF-ß signaling using a neutralizing antiTGF-ß1, -ß2, and -ß3 antibody accelerates the development of atherosclerotic lesions in apoE-deficient mice. Moreover, inhibition of TGF-ß signaling favors the development of lesions with increased inflammatory component and decreased collagen content. These results identify a major protective role for TGF-ß in atherosclerosis.
Key Words: atherosclerosis cytokines inflammation macrophages lymphocytes
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