July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Endoplasmic reticulum stress decreases mitochondrial membrane potential and upregulates PARK2 expression in corneal endothelium
Author Affiliations & Notes
  • Takashi Miyai
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Tetsuya Toyono
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Kodai Kitamoto
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Masaya Fukushima
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Junko Yoshida
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Rika Shirakawa
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Suguru Nakagawa
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Ula V. Jurkunas
    Department of Ophthalmology, Schepens Eye Research Institute/ Massachusetts Eye and Ear/ Harvard Medical School, Boston, Massachusetts, United States
  • Tomohiko Usui
    Department of Ophthalmology, University of Tokyo, Bunkyo-ku, Tokyo, Japan
  • Footnotes
    Commercial Relationships   Takashi Miyai, None; Tetsuya Toyono, None; Kodai Kitamoto, None; Masaya Fukushima, None; Junko Yoshida, None; Rika Shirakawa, None; Suguru Nakagawa, None; Ula Jurkunas, None; Tomohiko Usui, Bonac (P), Senju (P)
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 4436. doi:
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    • Get Citation

      Takashi Miyai, Tetsuya Toyono, Kodai Kitamoto, Masaya Fukushima, Junko Yoshida, Rika Shirakawa, Suguru Nakagawa, Ula V. Jurkunas, Tomohiko Usui; Endoplasmic reticulum stress decreases mitochondrial membrane potential and upregulates PARK2 expression in corneal endothelium. Invest. Ophthalmol. Vis. Sci. 2018;59(9):4436.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : It is reported that endoplasmic reticulum stress (ER stress) is related to the pathogenesis of Fuchs endothelial corneal dystrophy (FECD) and that ER stress is associated with mitochondrial dysfunction and membrane potential decrease generally followed by mitophagy upregulation. However, these mechanisms have not been adequately investigated in corneal endothelium so far. The purpose of this study is to examine the relationship between ER stress and mitochondrial change in corneal endothelium.

Methods : Corneal endothelial cell line, HCEnC-21T, was treated with ER stressor thapsigargin with the concentration of 1, 2.5, 5, or 10 uM for 6 hours. Mitochondrial membrane potential was measured by JC-10 assay. After appropriate concentration was decided, we performed qRT-PCR with the primers of ER stress markers (CHOP, GRP78), mitophagy related genes (PINK1, PARK2), and mitochondrial anti-apoptotic gene Bcl2.

Results : JC-10 assay showed 10μM of thapsigargin reduced mitochondrial membrane potential. Compared with the controls, relative mRNA expression levels (ΔΔCT) of CHOP (58.5-fold), GRP78 (2.4-fold) and PARK2 (32.4-fold) were increased in HCEnC-21T cells with treatment of 10μM thapsigargin for 6 hours.

Conclusions : ER stress induced by thapsigargin decreased mitochondrial membrane potential and increase in ER stress markers and mitophagy-related gene PARK2. This data indicates that ER stress leads to mitochondrial dysfunction seen in FECD.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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