In Vivo Effect of TGF-β1

Author:

Kanzaki Tetsuto1,Tamura Ken1,Takahashi Kazuo1,Saito Yasushi1,Akikusa Bunshiro1,Oohashi Hideya1,Kasayuki Noriaki1,Ueda Makiko1,Morisaki Nobuhiro1

Affiliation:

1. From the Second Department of Internal Medicine (T.K., K. Tamura, K. Takahashi, Y.S., N.M.) and the Second Department of Pathology (B.A.), School of Medicine, Chiba University, Chiba; the Kirin Brewery Co, Ltd (H.O.), Maebashi City; and the Department of Pathology, Osaka City University Medical School (N.K., M.U.), Osaka, Japan.

Abstract

Abstract The in vivo effect of transforming growth factor–β1 (TGF-β1) was studied in a model system in which arterial intimal thickening was induced by injury of rabbit arteries with a balloon catheter (BCI). Intimal area and its ratio to medial area in carotid arteries after BCI were significantly higher in rabbits treated with 10 μg/kg TGF-β1 and 10 mg/kg aspirin IV QD (TGF-β1 group) than in those treated with 10 mg/kg aspirin IV QD only (control group). Intimal cell numbers in the TGF-β1 and control groups were not significantly different from each other, but matrix volume in the intimal layer was significantly higher in the TGF-β1 group. By immunohistochemical and Northern blot analyses, the fibronectin content in carotid intimal and medial layers was greater in the TGF-β1 group compared with that in the control group. Thus, in intimal thickenings induced by BCI, TGF-β1 mainly enhanced the formation of matrix containing fibronectin. Moreover, the mRNAs of TGF-β type I and type II receptors were detected in carotid arteries 7 and 14 days after, but not before, BCI. Thus, TGF-β1 influences the process of intimal thickening induced by BCI through a receptor-mediated mechanism in vivo. The significance of this fact is discussed in relation to the development of atherosclerosis.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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