Type 2 deiodinase expression is stimulated by growth factors in human vascular smooth muscle cells

被引：15

作者：

Maeda, A ^{[1
]}

Toyoda, N ^{[1
]}

Yasuzawa-Amano, S ^{[1
]}

Iwasaka, T ^{[1
]}

Nishikawa, M ^{[1
]}

机构：

[1] Kansai Med Univ, Dept Med 2, Moriguchi, Osaka 570, Japan

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2003年 / 200卷 / 1-2期

关键词：

thyroid hormone; deiodinase; vascular smooth muscle cell; platelet-derived growth factor; basic fibroblast growth factor;

D O I：

10.1016/S0303-7207(02)00409-4

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Type 2 deiodinase (D2) catalyzes the conversion of the prohormone T4 to the biologically active T3. D2 is expressed in human aortic smooth muscle cells (hASMCs). In this study, we demonstrated that the D2 mRNA and activity in hASMCs were up-regulated by platelet-derived growth factor-BB (PDGF-BB) and basic fibroblast growth factor (bFGF). The induction of D2 mRNA by PDGF-BB and bFGF was dependent on de novo RNA and protein synthesis. PD98059, a specific inhibitor of the upstream kinase that activates extracellular signal-regulated kinase (ERK), significantly suppressed the induction by both PDGFBB and bFGF. SB203580, a specific inhibitor of p38 mitogen-activated protein (MAP) kinase, and SP600125, a specific inhibitor of c-Jun N-terminal kinase (JNK), also reduced the induction by both PDGF-BB and bFGF. These results suggest that both PDGFBB and bFGF induce D2 expression at least partly via ERK pathway. The p38 MAP kinase and JNK pathways may also be involved in the induction. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：111 / 117

页数：7

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