Li Ying, Jin Rujun, Li Lan, Choi Ji Suk, Kim Jonghwa, Yoon Hyeon Jeong, Park Jong Hwan, Yoon Kyung Chul
Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea.
Department of Biomedical Sciences and Centers for Creative Biomedical Scientists, Chonnam National University, Gwangju 61469, Korea.
Int J Mol Sci. 2021 Feb 18;22(4):2015. doi: 10.3390/ijms22042015.
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.
在本研究中，我们调查了蓝光照射对小鼠眼表核苷酸结合寡聚化结构域2（NOD2）表达的影响，并评估了NOD2激活在光诱导细胞死亡中的作用。将小鼠分为野生型（WT）、NOD2基因敲除（KO）、WT+蓝光（WT+BL）和NOD2-KO+蓝光（NOD2-KO+BL）组，WT+BL组和NOD2-KO+BL组的小鼠接受10天蓝光照射。蓝光照射10天后，在WT+BL组和NOD2-KO+BL组中观察到活性氧和丙二醛增加，WT+BL组显示出更高的NOD2和自噬相关16样蛋白1的表达。虽然WT+BL组和NOD2-KO+BL组的轻链3-II表达均增加，但NOD2-KO+BL组小鼠的p62表达明显低于WT+BL组小鼠。此外，NOD2-KO+BL组小鼠的角膜上皮损伤和凋亡明显低于WT+BL组小鼠。总之，蓝光照射可通过激活眼表的NOD2诱导自噬受损。此外，活性氧（ROS）-NOD2-自噬相关16样蛋白1（ATG16L）信号通路可能参与蓝光诱导的自噬反应，导致角膜上皮凋亡。
