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Protective effects of autophagy against blue light-induced retinal degeneration in aged mice

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Abstract

The aim of this study was to explore the role of autophagy in response to blue light damage in aged mice and in human retinal pigmented epithelium (hRPE) cells. Blue light damage to the retina was induced in 10-month-old (10 mo) C57 mice and hRPE cells. Flash electroretinography was used to assess retinal function. Retinal structure changes were observed by electron microscopy. Western blot was conducted to determine the expression levels of the following proteins: cleaved caspase-3, p38 mitogen-activated protein kinases, protein kinase R-like endoplasmic reticulum kinase (PERK), autophagy marker light chain 3 (LC3), P62, and Beclin-1. On day 1 after light damage to the 10 mo mice, retinal function was changed. The latent periods of a-wave and b-wave were delayed, and amplitude was reduced. The electron microscopy results revealed mitochondria damage in the retinal pigmented epithelium and a disorganized photoreceptor outer segment (OS). PERK, LC3, and Beclin-1 were upregulated, whereas P62 was not. On day 5 after the blue light damage, restoration of electroretinography and OS was observed. PERK, LC3, and Beclin-1 were downregulated, whereas P62 was not. Protein changes in vitro were consistent with in vivo. The present study provided structural and functional evidence that autophagy plays an important role in the response to blue lightinduced retinal damage.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (81470649,81670870) and the Beijing Nova Program (Z161100004916058). The organizations that funded this study had no role in the study design, data collection, and analysis or in the decision to publish or prepare the manuscript.

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Correspondence to Lvzhen Huang or Xiaoxin Li.

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Xia, H., Hu, Q., Li, L. et al. Protective effects of autophagy against blue light-induced retinal degeneration in aged mice. Sci. China Life Sci. 62, 244–256 (2019). https://doi.org/10.1007/s11427-018-9357-y

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  • DOI: https://doi.org/10.1007/s11427-018-9357-y

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