PTX3, a key component of innate immunity, is induced by SAA via FPRL1-mediated signaling in HAECs.

Publisher: Wiley-Liss Country of Publication: United States NLM ID: 8205768 Publication Model: Print Cited Medium: Internet ISSN: 1097-4644 (Electronic) Linking ISSN: 07302312 NLM ISO Abbreviation: J Cell Biochem Subsets: MEDLINE

Publication: <2004>- : Hoboken, NJ : Wiley-Liss
Original Publication: New York : Liss, c1982-

Aorta/*metabolism ; C-Reactive Protein/*biosynthesis ; Endothelial Cells/*metabolism ; Immunity, Innate/*drug effects ; Receptors, Formyl Peptide/*metabolism ; Receptors, Lipoxin/*metabolism ; Serum Amyloid A Protein/*pharmacology ; Serum Amyloid P-Component/*biosynthesis ; Signal Transduction/*drug effects; Aorta/immunology ; Atherosclerosis/genetics ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; C-Reactive Protein/genetics ; C-Reactive Protein/immunology ; Cell Line ; Dose-Response Relationship, Drug ; Endothelial Cells/immunology ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Gene Expression Regulation/immunology ; Humans ; Immunity, Innate/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/immunology ; MAP Kinase Kinase 4/metabolism ; NF-kappa B/genetics ; NF-kappa B/immunology ; NF-kappa B/metabolism ; Receptors, Formyl Peptide/genetics ; Receptors, Formyl Peptide/immunology ; Receptors, Lipoxin/genetics ; Receptors, Lipoxin/immunology ; Recombinant Proteins/genetics ; Recombinant Proteins/immunology ; Recombinant Proteins/metabolism ; Recombinant Proteins/pharmacology ; Serum Amyloid A Protein/genetics ; Serum Amyloid A Protein/immunology ; Serum Amyloid A Protein/metabolism ; Serum Amyloid P-Component/genetics ; Serum Amyloid P-Component/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Transcription Factor AP-1/genetics ; Transcription Factor AP-1/immunology ; Transcription Factor AP-1/metabolism

Serum amyloid A (SAA) is regarded as an important acute phase protein in coronary artery diseases. However, its involvement in the immune response of atherosclerosis is poorly understood. The present study was designed to investigate the influence of SAA on the secretion of long pentraxin 3 (PTX3), a key component of innate immunity, in human aortic endothelial cells (HAECs). Our study revealed that recombinant SAA up-regulated PTX3 production in a remarkable dose- and time-dependent manner and the activation of formyl peptide receptor-like 1 (FPRL1) was crucial for SAA-induced expression of PTX3 in HAECs. Meanwhile, SAA-induced PTX3 production could be significantly down-regulated by using the specific siRNA sequences for Jun N-terminal kinases (JNK). Furthermore, the activation of activator protein-1 (AP-1) was necessary for the up-regulation of PTX3 expression. We also found that the activation of nuclear factor-kappa B (NF-κB) played an important role in this process. Our findings demonstrate that SAA up-regulates PTX3 production via FPRL1 significantly, and thus, contributes to the inflammatory pathogenesis of atherosclerosis.
(copyright © 2011 wiley-liss, inc.)

0 (FPR2 protein, human)
0 (NF-kappa B)
0 (Receptors, Formyl Peptide)
0 (Receptors, Lipoxin)
0 (Recombinant Proteins)
0 (Serum Amyloid A Protein)
0 (Serum Amyloid P-Component)
0 (Transcription Factor AP-1)
148591-49-5 (PTX3 protein)
9007-41-4 (C-Reactive Protein)
EC 2.7.12.2 (MAP Kinase Kinase 4)

Date Created: 20110406 Date Completed: 20111102 Latest Revision: 20110713

20221213

10.1002/jcb.23128

21465531