title: Human retinal pigment epithelial cells express the long pentraxin PTX3.
abstract: OBJECTIVE
  To determine whether the long pentraxin 3 (PTX3) is expressed in human retinal pigment epithelial cells and is induced by inflammatory cytokines, interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ), expression of PTX3 was investigated in the human retinal pigment epithelial cell line, ARPE-19 cells.
  
  
  METHODS
  In ARPE-19 cells, we first analyzed PTX3 production in the presence or absence of inflammatory cytokines, IL-1β, TNF-α, and IFN-γ, dose- and time-dependently using enzyme-linked immunosorbent assay. Protein and mRNA expression of PTX3 was measured with western blotting analysis and real-time reverse transcription-polymerase chain reaction. Specific inhibitors were used to determine the signaling pathways of inflammatory cytokine-induced PTX3 expression.
  
  
  RESULTS
  In this study, production of PTX3 was induced by IL-1β and TNF-α dose- and time-dependently, but not by IFN-γ in ARPE-19 cells. Protein and mRNA expression of PTX3 was significantly upregulated in the presence of IL-1β and TNF-α. Furthermore, pretreatment with extracellular signal-regulated kinase1/2 and nuclear factor kappa-light-chain-enhancer of activated B cells specific inhibitor abolished IL-1β and TNF-α-induced PTX3 production, but the other inhibitors had no effect.
  
  
  CONCLUSIONS
  These results suggested that human retinal pigment epithelial cells may be a major source of PTX3 production in the presence of proinflammatory cytokines, IL-1β and TNF-α, and could be an important mediator for host defense and inflammatory response in the retina. The importance of the mitogen-activated protein kinase/extracellular signal-regulated kinase1/2 and nuclear factor kappa-light-chain-enhancer of activated B cells pathways for regulated PTX3 expression may be a potential target for PTX3 regulation in the retina.
authors: Department of Opthalmology, Ulsan University Hospital, Ulsan, South Korea.
authors: Je Moon
authors: JM
authors: Woo
authors: Min-Young
authors: MY
authors: Kwon
authors: Da-Yong
authors: DY
authors: Shin
authors: Young-Ho
authors: YH
authors: Kang
authors: Narae
authors: N
authors: Hwang
authors: Su Wol
authors: SW
authors: Chung
mesh_terms: D000873:Anthracenes / Q000494:pharmacology; D002070:Butadienes / Q000494:pharmacology; D002097:C-Reactive Protein / Q000235:genetics* / Q000378:metabolism*; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D009570:Nitriles / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D055213:Retinal Pigment Epithelium / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D000683:Serum Amyloid P-Component / Q000235:genetics* / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D013450:Sulfones / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000099153:Pentraxins
chemical_list: D000873:Anthracenes; D002070:Butadienes; D002097:C-Reactive Protein; D016207:Cytokines; D007093:Imidazoles; D018836:Inflammation Mediators; D007371:Interferon-gamma; D053583:Interleukin-1beta; D016328:NF-kappa B; D009570:Nitriles; D011725:Pyridines; D012333:RNA, Messenger; D000683:Serum Amyloid P-Component; D013450:Sulfones; D014409:Tumor Necrosis Factor-alpha; D000099153:Pentraxins; C416282:BAY 11-7085; C113580:U 0126; C432165:pyrazolanthrone; C093642:SB 203580
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