Transforming growth factor-β1 induces the non-classical secretion of peroxiredoxin-I in A549 cells

被引：40

作者：

Chang, Jong Wook ^{[1
]}

Lee, Seung Hee ^{[1
]}

Lu, Yan ^{[1
]}

Yoo, Yung Joon ^{[1
]}

机构：

[1] Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 345卷 / 01期

关键词：

peroxiredoxin-I; ER/golgi-independent secretory pathway; non-classical secretion; A549; cells; TGF-beta; 1; furin;

D O I：

10.1016/j.bbrc.2006.04.073

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：

Recent studies found that peroxiredoxin-I (Prx-I) is secreted from A549 cells although it does not contain a signal peptide and is known to be a cytosolic protein. Transforming growth factor-beta 1 (TGF-beta 1) treatment dramatically enhanced Prx-I secretion from A549 cells, and this effect was not inhibited by brefeldin A. Further investigation revealed that A549 cells constitutively secrete TGF-beta 1. Furin, a TGF-beta 1-converting enzyme, was also highly activated in A549 cells. Ectopic expression of alpha(1)-antitrypsin Portland (alpha(1)-PDX), a potent furin inhibitor, blocked both TGF-beta 1 activation and Prx-I secretion. Our findings collectively suggest that nonclassical secretion of Prx-I is induced by TGF-beta 1, which is constitutively activated by furin in A549 cells. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：118 / 123

页数：6

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