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Blue Light Induces Impaired Autophagy through Nucleotide-Binding Oligomerization Domain 2 Activation on the Mouse
Ying Li1, Rujun Jin1, Lan Li1,2
1Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea.
Abstract:
In this study, we investigated the effects of blue light exposure on nucleotide-binding oligomerization domain 2 (NOD2) expression on the mouse ocular surface and evaluated the role of NOD2 activation in light-induced cell death. Mice were divided into wild-type (WT), NOD2-knock out (KO), WT + blue light (WT + BL), and NOD2-KO + blue light (NOD2-KO + BL) groups, and the mice in the WT+BL and NOD2-KO + BL groups were exposed to blue light for 10 days. After 10 days of blue light exposure, increased reactive oxygen species and malondialdehyde were observed in the WT + BL and NOD2-KO + BL groups, and the WT + BL group showed a higher expression of NOD2 and autophagy related 16 like 1. Although both WT+BL and NOD2-KO + BL groups showed an increase in the expression of light chain 3-II, NOD2-KO + BL mice had a significantly lower p62 expression than WT + BL mice. In addition, NOD2-KO+BL mice had significantly lower corneal epithelial damage and apoptosis than WT + BL mice. In conclusion, blue light exposure can induce impaired autophagy by activation of NOD2 on the ocular surface. In addition, the reactive oxygen species (ROS)-NOD2-autophagy related 16 like 1 (ATG16L) signaling pathway may be involved in the blue-light-induced autophagy responses, resulting in corneal epithelial apoptosis.
Insights
Blue light exposure harms the ocular surface by activating nucleotide-binding oligomerization domain 2 (NOD2), leading to impaired autophagy and cell death. NOD2 knockout mice showed reduced damage, suggesting NOD2
Area of Science:
- Ophthalmology
- Cell Biology
- Molecular Biology
Background:
- Blue light exposure is a growing concern for ocular health.
- Nucleotide-binding oligomerization domain 2 (NOD2) plays a role in immune responses.
- Autophagy is a critical cellular process for maintaining homeostasis.
Purpose of the Study:
- To investigate the effect of blue light on NOD2 expression in the mouse ocular surface.
- To evaluate the role of NOD2 activation in blue light-induced ocular cell death.
- To elucidate the signaling pathway involved in blue light-induced ocular damage.
Main Methods:
- Comparison of wild-type (WT) and NOD2-knockout (KO) mice.
- Exposure of mice to blue light (BL) for 10 days.
- Measurement of reactive oxygen species (ROS), malondialdehyde, NOD2, autophagy markers (ATG16L, LC3-II, p62), corneal epithelial damage, and apoptosis.
Main Results:
- Blue light exposure increased ROS and malondialdehyde in both WT and NOD2-KO mice.
- WT mice exposed to blue light showed higher NOD2 and ATG16L expression.
- NOD2-KO mice exhibited significantly less corneal epithelial damage and apoptosis compared to WT mice after blue light exposure.
- The ROS-NOD2-ATG16L pathway was implicated in blue light-induced autophagy and apoptosis.
Conclusions:
- Blue light exposure induces ocular surface damage by activating NOD2.
- NOD2 activation leads to impaired autophagy and subsequent corneal epithelial apoptosis.
- The ROS-NOD2-ATG16L signaling pathway is crucial in mediating blue light-induced ocular surface injury.
