Transforming growth factor-β1 induces the non-classical secretion of peroxiredoxin-I in A549 cells
Transforming growth factor-β1 induces the non-classical secretion of peroxiredoxin-I in A549 cells
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DOI：
10.1016/j.bbrc.2006.04.073
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发表时间：
2006-06-23
影响因子：
3.1
通讯作者：
Yoo, Yung Joon
中科院分区：
文献类型：
--
作者：
Chang, Jong Wook;Lee, Seung Hee;Yoo, Yung Joon
最近的研究发现，虽然Prx-I不含信号肽，但它是一种胞质蛋白，由A549细胞分泌。转化生长因子- β 1 （tgf - β 1）处理显著提高了A549细胞的prx - 1分泌，而这种作用不受brefeldin a的抑制。进一步的研究表明，A549细胞组成性地分泌tgf - β 1。Furin，一种tgf - β 1转化酶，在A549细胞中也被高度激活。α(1)-抗胰蛋白酶波特兰（α (1)-PDX）是一种有效的糠蛋白抑制剂，其异位表达可阻断tgf - β 1的激活和Prx-I的分泌。我们的研究结果共同表明，Prx-I的非经典分泌是由tgf - β 1诱导的，而tgf - β 1在A549细胞中被furin组成性激活。(c) 2006爱思唯尔公司版权所有。
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.