Article

Activation of formyl peptide receptor like-1 by serum amyloid A induces CCL2 production in human umbilical vein endothelial cells.

Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
Biochemical and Biophysical Research Communications (Impact Factor: 2.28). 02/2009; 380(2):313-7. DOI: 10.1016/j.bbrc.2009.01.068
Source: PubMed

ABSTRACT We investigated the effects of serum amyloid A (SAA) on the production of C-C chemokine motif ligand 2 (CCL2) and the mechanism underlying SAA action in human umbilical vein endothelial cells (HUVECs). Stimulation of HUVECs by SAA elicited CCL2 production in a concentration-dependent manner. SAA induced the activations of NF-kappaB and AP-1, which were essential for CCL2 production after SAA stimulation. HUVECs expressed formyl peptide receptor-like 1 (FPRL1), and short interfering RNA knockdown of FPRL1 nearly completely blocked SAA-induced CCL2 production in HUVECs. We suggest that SAA stimulates CCL2 production via FPRL1 and, thus, contributes to atherosclerosis.

0 Bookmarks
 · 
66 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Elevated levels of serum amyloid A (SAA) is a risk factor for cardiovascular diseases, however, the role of SAA in the pathophysiology of atherosclerosis remains unclear. Here we show that SAA induced macrophage foam cell formation. SAA-stimulated foam cell formation was mediated by c-jun N-terminal kinase (JNK) signaling. Moreover, both SAA and SAA-conjugated high density lipoprotein stimulated the expression of the important scavenger receptor lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) via nuclear factor-κB (NF-κB). A LOX1 antagonist carrageenan significantly blocked SAA-induced foam cell formation, indicating that SAA promotes foam cell formation via LOX1 expression. Our findings therefore suggest that SAA stimulates foam cell formation via LOX1 induction, and thus likely contributes to atherogenesis.
    Biochemical and Biophysical Research Communications 02/2013; · 2.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recently we demonstrated that SAA induces macrophage foam cell formation. In this study we show that SAA-induced foam cell formation is inhibited by formyl peptide receptor 2 (FPR2) antagonist WRW(4), as well as by FPR2-targeted siRNA knockdown. SAA-stimulated LOX1 expression was also mediated by FPR2. We also found that SAA-stimulated foam cell formation and LOX1 expression was pertussis toxin-insensitive. In addition, FPR2 is upregulated in peripheral blood mononuclear cells from patients with atherosclerosis. Our findings therefore suggest that SAA stimulates foam cell formation via FPR2 signaling and LOX1 induction, and thus likely contributes to atherogenesis.
    Biochemical and Biophysical Research Communications 03/2013; · 2.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Glial cells, a close partner to neurons, are able to communicate with each other and with neurons through secreted proteins and other molecules. Secreted proteins in the extracellular environment probably play a direct role in the control and regulation of numerous biological and disease processes in the nervous system. Provision of precise diagnosis and prognosis to patients with a neurological disorder is problematic. Glial activation is a hallmark of every type of injury to the nervous system. In these circumstances, it is the glial biomarker whose development and implementation can be the most suitable approach to assessment of neuroinflammation and neurotoxicity. Here, the importance of glial secreted proteins as diagnostic/prognostic biomarkers and their functional contribution to regulation of neuroinflammation are reviewed. Evidence for the use of glia-based biomarkers for improvement of diagnostic and prognostic accuracy is also summarized and recommendations for future glia-based biomarker research are provided.
    Expert Review of Proteomics 02/2013; 10(1):43-63. · 3.90 Impact Factor