Serum amyloid A stimulates matrix-metalloproteinase-9 upregulation via formyl peptide receptor like-1-mediated signaling in human monocytic cells
Serum amyloid A stimulates matrix-metalloproteinase-9 upregulation via formyl peptide receptor like-1-mediated signaling in human monocytic cells
复制标题
DOI：
10.1016/j.bbrc.2005.03.069
复制
发表时间：
2005-05-13
影响因子：
3.1
通讯作者：
Bae, YS
中科院分区：
文献类型：
--
作者：
Lee, HY;Kim, MK;Bae, YS
在本研究中，我们发现，血清淀粉样蛋白A（SAA）刺激基质金属蛋白酶-9（MMP-9）在THP-1细胞的转录和翻译水平上调。SAA刺激核因子κ B（NF-κ B）的活化，这是SAA上调MMP-9所必需的。SAA诱导的信号传导事件包括ERK激活和细胞内钙升高，这是MMP-9上调所必需的。甲酰肽受体样1（FPRL 1）被发现参与SAA上调MMP-9。在几种FPRL 1激动剂中，包括Trp-Lys-Tyr-Met-Val-D-Met（WKYMVm），SAA选择性刺激MMP-9上调。关于SAA和WKYMVm差异作用的分子机制，我们发现SAA不能竞争性抑制I-125标记的WKYMVm与FPRL 1的结合。总而言之，我们认为SAA通过诱导人单核细胞中MMP-9上调，在通过FPRL 1调节炎症和免疫反应中发挥作用。(c)2005年爱思唯尔公司All rights reserved.
In the present study, we found that serum amyloid A (SAA) stimulated matrix-metalloproteinase-9 (MMP-9) upregulation at the transcription and translational levels in THP-1 cells. SAA stimulated the activation of nuclear factor kappa B (NF-kappa B), which was required for the MMP-9 upregulation by SAA. The signaling events induced by SAA included the activation of ERK and intracellular calcium rise, which were found to be required for MMP-9 upregulation. Formyl peptide receptor like 1 (FPRL1) was found to be involved in the upregulation of MMP-9 by SAA. Among several FPRL1 agonists, including Trp-Lys-Tyr-Met-Val-D-Met (WKYMVm), SAA selectively stimulated MMP-9 upregulation. With respect to the molecular mechanisms involved in the differential action of SAA and WKYMVm, we found that SAA could not competitively inhibit the binding of I-125-labeled WKYMVm to FPRL1. Taken together, we suggest that SAA plays a role in the modulation of inflammatory and immune responses via FPRL1, by inducing MMP-9 upregulation in human monocytic cells. (c) 2005 Elsevier Inc. All rights reserved.