DcR3 protects THP-1 macrophages from apoptosis by increasing integrin α4

被引：24
|
作者：
Tateishi, Koji [2 ]
Miura, Yasushi [1 ,2 ]
Hayashi, Shinya [2 ]
Takahashi, Masayasu [2 ]
Kurosaka, Masahiro [2 ]
机构：
[1] Kobe Univ, Grad Sch Hlth Sci, Dept Rehabil Sci, Suma Ku, Kobe, Hyogo 6540142, Japan
[2] Kobe Univ, Grad Sch Med, Dept Orthopaed Surg, Kobe, Hyogo 6540142, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 389卷 / 04期
关键词：
Rheumatoid arthritis; Decoy receptor 3; Macrophage; Apoptosis; Adhesion molecule; RHEUMATOID-ARTHRITIS; DECOY RECEPTOR; FAS LIGAND; T-CELL; AMPLIFICATION; FIBRONECTIN; FIBROBLAST; ADHESION; P53; DIFFERENTIATION;
D O I：
10.1016/j.bbrc.2009.09.027
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：
In order to analyze the function of DcR3 for the regulation of cell adhesion and apoptosis in macrophages, we investigated the expression of decoy receptor 3 (DcR3) in THP-1 monocytes/macrophages. DcR3 was expressed in THP-1 and increased by phorbol 12-myristate 13-acetate (PIVIA). The formation of macrophage aggregates was observed when THP-1 cells were differentiated by PMA or stimulated with DcR3-Fc. Undifferentiated THP-1 cells were also induced to form aggregates by DcR3-Fc. The expression of integrin alpha 4 was significantly increased by DcR3-Fc. CHX-induced apoptosis in THP-1 was inhibited by DcR3-Fc, of which inhibition against CHX-induced apoptosis and aggregate formation were ameliorated by anti-VLA4 antibody. DcR3 may play a significant role in macrophages not only by a decoy receptor but also by increasing a4 integrin. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码：593 / 598
页数：6
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