Investigative Ophthalmology & Visual Science Cover Image for Volume 62, Issue 8
June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
Blue light induces impaired autophagy through nucleotide-binding oligomerization domain 2 activation on the mouse ocular surface
Author Affiliations & Notes
  • Ying Li
    Chonnam National University, Gwangju, Jeollanam-do, Korea (the Republic of)
  • Rujun Jin
    Chonnam National University, Gwangju, Jeollanam-do, Korea (the Republic of)
  • Lan Li
    Chonnam National University, Gwangju, Jeollanam-do, Korea (the Republic of)
  • Jonghwa Kim
    Chonnam National University, Gwangju, Jeollanam-do, Korea (the Republic of)
  • Hyeon Jeong Yoon
    Chonnam National University, Gwangju, Jeollanam-do, Korea (the Republic of)
  • Kyung Chul Yoon
    Chonnam National University, Gwangju, Jeollanam-do, Korea (the Republic of)
  • Footnotes
    Commercial Relationships   Ying Li, None; Rujun Jin, None; Lan Li, None; Jonghwa Kim, None; Hyeon Jeong Yoon, None; Kyung Chul Yoon, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 1300. doi:
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      Ying Li, Rujun Jin, Lan Li, Jonghwa Kim, Hyeon Jeong Yoon, Kyung Chul Yoon; Blue light induces impaired autophagy through nucleotide-binding oligomerization domain 2 activation on the mouse ocular surface. Invest. Ophthalmol. Vis. Sci. 2021;62(8):1300.

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

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Abstract

Purpose : To investigate the effect of blue light (BL) exposure on nucleotide-binding oligomerization domain 2 (NOD2) expression on the mouse ocular surface and to evaluate the role of NOD2 signaling in BL-induced cell death.

Methods : Wild or NOD2 knock-out (KO) C57BL/6 mice were exposed to BL (410nm) twice a day for 10 days at an energy capacity of 100 J/cm2 and divided into the WT+BL and NOD2-KO+BL groups. Mice in the WT and NOD2-KO groups were not exposed to BL and served as control. Corneal fluorescein staining scores were measured after 10 days of BL stimulation. 2’7’-dichlorofluorescein diacetate for reactive oxygen species (ROS), enzyme-linked immunosorbent assay for malondialdehyde (MDA), and terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling for apoptosis were performed 10 days after exposure to BL. In addition, expression of NOD2, ATG16L1, LC3-∥, and p62 were evaluated using Western blot.

Results : After exposure to BL, increased ROS and MDA were observed in the WT+BL and NOD2-KO+BL groups, and the WT+BL group showed a higher expression of NOD2 and ATG16L. Mice in the WT+BL and NOD2-KO+BL groups showed a significant increase in the expression of LC3-∥ and p62, whereas the NOD2-KO+BL mice had lower LC3-∥ expression and higher p62 expression compared to WT+BL mice. In addition, NOD2-KO+BL mice had significantly lower corneal epithelial damage and apoptosis than WT+BL mice.

Conclusions : BL exposure can induce impaired autophagy by activation of NOD2 on the ocular surface. In addition, the ROS-NOD2-ATG16L signaling pathway may be involved in the BL-induced autophagy responses, resulting in corneal epithelial apoptosis.

This is a 2021 ARVO Annual Meeting abstract.

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