Role of PKC and TGF-β receptor in glucose-induced proliferation of smooth muscle cells

被引：28

作者：

Yasuda, Y ^{[1
]}

Nakamura, J ^{[1
]}

Hamada, Y ^{[1
]}

Nakayama, M ^{[1
]}

Chaya, S ^{[1
]}

Naruse, K ^{[1
]}

Nakashima, E ^{[1
]}

Kato, K ^{[1
]}

Kamiya, H ^{[1
]}

Hotta, N ^{[1
]}

机构：

[1] Nagoya Univ, Sch Med, Dept Internal Med 3, Nagoya, Aichi 466, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 281卷 / 01期

关键词：

aortic smooth muscle cells; protein kinase C; transforming growth factor-beta; transforming growth factor-beta receptor; diabetic macroangiopathy;

D O I：

10.1006/bbrc.2001.4310

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The role of protein kinase C (PKC) and transforming growth factor (TGF)-beta in the proliferation of vascular smooth muscle cells (SMCs) under a high glucose condition was investigated. [H-3]-thymidine incorporation under 20 mM glucose was significantly accelerated compared with that under 5.5 mM glucose, and this increase was inhibited by an anti-TGF-beta antibody or a PKC-beta specific inhibitor, LY333531. The amount of active and total TGF-beta1 in the conditioned media did not differ between 5.5 and 20 mM glucose. However, the expression of TGF-beta receptor type II under 20 mM glucose was significantly increased, but that of the TGF-beta receptor type I was not. This increased expression of the TGF-beta receptor type II was prevented by LY333531. These observations suggest that the increased expression of the TGF-beta receptor type II via PKC-beta plays an important role in the accelerated proliferation of SMCs under a high glucose condition, leading to the development of diabetic macroangiopathy. (C) 2001 Academic Press.

引用

页码：71 / 77

页数：7

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