title: Tunicamycin-induced Endoplasmic Reticulum Stress Upregulates the Expression of Pentraxin 3 in Human Retinal Pigment Epithelial Cells.
abstract: OBJECTIVE
  To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19.
  
  
  METHODS
  PTX3 production in ARPE-19 cells was analyzed in the absence or presence of tunicamycin treatment by enzyme-linked immunosorbent assay. PTX3 protein and mRNA levels were estimated using western blot analysis and real-time reverse transcription-polymerase chain reaction, respectively. Protein and mRNA levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measured in the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfected ARPE-19 cells.
  
  
  RESULTS
  The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment. PTX3 production was significantly decreased in inositol-requiring enzyme 1α shRNA-transfected ARPE-19 cells compared to control shRNA-transfected cells. Furthermore, pretreatment with the NF-κB inhibitor abolished tunicamycin-induced PTX3 production. Decreased cell viability and prolonged protein and mRNA expression of CHOP were observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells.
  
  
  CONCLUSIONS
  These results suggest that PTX3 production increased in the presence of tunicamycin-induced ER stress. Therefore, PTX3 could be an important protector of ER stress-induced cell death in human retinal pigment epithelial cells. Inositol-requiring enzyme 1α and the NF-κB signaling pathway may serve as potential targets for regulation of PTX3 expression in the retina. Therefore, their role in PTX3 expression needs to be further investigated.
authors.affiliation: School of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan, Korea.
authors.forename: Narae
authors.initials: N
authors.lastname: Hwang
authors.affiliation: School of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan, Korea.
authors.forename: Min-Young
authors.initials: MY
authors.lastname: Kwon
authors.affiliation: Department of Ophthalmology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.
authors.forename: Jae Bong
authors.initials: JB
authors.lastname: Cha
authors.affiliation: School of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan, Korea.
authors.forename: Su Wol
authors.initials: SW
authors.lastname: Chung
authors.affiliation: Department of Ophthalmology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.
authors.forename: Je Moon
authors.initials: JM
authors.lastname: Woo
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D017209:Apoptosis; D015153:Blotting, Western; D002097:C-Reactive Protein / Q000096:biosynthesis / Q000235:genetics*; D002478:Cells, Cultured; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects* / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation; D006801:Humans; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics*; D055213:Retinal Pigment Epithelium / Q000378:metabolism* / Q000473:pathology; D000683:Serum Amyloid P-Component / Q000096:biosynthesis / Q000235:genetics*; D014415:Tunicamycin / Q000494:pharmacology*; D000099153:Pentraxins
chemical_list: D000900:Anti-Bacterial Agents; D002097:C-Reactive Protein; D012333:RNA, Messenger; D000683:Serum Amyloid P-Component; D014415:Tunicamycin; D000099153:Pentraxins
keywords: Endoplasmic reticulum stress; Human retinal pigment epithelial cells; Inositol-requiring enzyme 1α; Pentraxin 3