title: PTX3, a key component of innate immunity, is induced by SAA via FPRL1-mediated signaling in HAECs.
abstract: 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.
authors.affiliation: The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University Qilu Hospital, Jinan, Shandong 250012, China.
authors.forename: Zhe
authors.initials: Z
authors.lastname: Dong
authors.forename: Fengling
authors.initials: F
authors.lastname: An
authors.forename: Tingting
authors.initials: T
authors.lastname: Wu
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhang
authors.forename: Mingxiang
authors.initials: M
authors.lastname: Zhang
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhang
authors.forename: Guipeng
authors.initials: G
authors.lastname: An
authors.forename: Fengshuang
authors.initials: F
authors.lastname: An
mesh_terms: D001011:Aorta / Q000276:immunology / Q000378:metabolism*; D050197:Atherosclerosis / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D002097:C-Reactive Protein / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000276:immunology / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects* / Q000276:immunology; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D048670:MAP Kinase Kinase 4 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D044042:Receptors, Formyl Peptide / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D044067:Receptors, Lipoxin / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D011994:Recombinant Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology; D000685:Serum Amyloid A Protein / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D000683:Serum Amyloid P-Component / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics / Q000276:immunology; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D048670:MAP Kinase Kinase 4; D016328:NF-kappa B; D044042:Receptors, Formyl Peptide; D044067:Receptors, Lipoxin; D011994:Recombinant Proteins; D000685:Serum Amyloid A Protein; D000683:Serum Amyloid P-Component; D018808:Transcription Factor AP-1; D000099153:Pentraxins; C105101:FPR2 protein, human