タカハシ カンジ   TAKAHASHI KANJI
  髙橋 寛二
   所属   関西医科大学  眼科学講座
   職種   非常勤講師
言語種別 英語
発表タイトル Altered expression of tight junctions in APRE19 cells under endoplasmic reticulum stress
会議名 Association for Reseach in Vision and Ophthalmology
学会区分 国際学会及び海外の学会
発表者・共同発表者◎Yoshikawa T, Ogata N, Izuta H , Shimazawa M, Hara H, Takahashi K
発表年月日 2010/05
開催地
(都市, 国名)
Fort Lauderdale,Florida
概要 Abstract Purpose:
Endoplasmic reticulum (ER) stress has been linked to the pathogenesis of the several diseases,e.g.. diabetes mellitus and Parkinson disease. ER stress induces the expression of inflammatory cytokines, and inflammatory cytokines have been reported to be the leading cause of diabetic retinopathy (DR) and age-related macular degeneration (AMD). Because retinal pigment epithelial (RPE) cells are associated with the development and pathogenesis of DR and AMD, we investigated the expression of tight junctions, and angiogenic and /anti- angiogenic factors in RPE cells under ER stress in vitro.
Material and Methods:ER stress was induced in cultured ARPE19 cells , a human retinal pigment epithelium cell line, by exposure to tunicamycin (TM; 1μg/ml) to inhibit N-linked glycosylation or thapsigargin (TG; 1μM) to inhibit the sarcoplasmic/endoplasmic calcium-ATPase. After 6, 12, 24, and 48 hours exposure, RNAs were extracted from the ARPE cells. The expressions of; GRP78/Bip (Bip) and C/EBP-homologous protein (CHOP) , markers of ER stress; zonula occluden (ZO)-1, occludin, and claudin1, genes for tight junctions; and vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) were determined by real time RT-PCR.
Conclusions:The increased expression of tight junctions and VEGF in TM- or TG-exposed ARPE19 cells indicate that the ER stress can alter the function of RPE cells and may be involved in the pathogenesis of DR and AMD.