NLRP3 Deficiency Attenuates Secondary Degeneration of Visual Cortical Neurons Following Optic Nerve Injury

  • Zhou Zhang
  • Wenyi Liu
  • Yubin Huang
  • Linlin Luo
  • Xiaofeng Cai
  • Yunjia Liu
  • Liqianyu Ai
  • Jun Yan
  • Sen LinEmail author
  • Jian YeEmail author
Original Article


In the visual pathway, optic nerve (ON) injury may cause secondary degeneration of neurons in distal regions, such as the visual cortex. However, the role of the neuroinflammatory response in regulating secondary impairment in the visual cortex after ON injury remains unclear. The NOD-like receptor family pyrin domain containing 3 (NLRP3) is an important regulator of neuroinflammation. In this study, we established a mouse model of unilateral ON crush (ONC) and showed that the expression of NLRP3 was significantly increased in the primary visual cortex (V1) as a response to ONC and that the NLRP3 inflammasome was activated in the contralateral V1 1 days–14 days after ONC. Ablation of the NLRP3 gene significantly decreased the trans-neuronal degeneration within 14 days. Visual electrophysiological function was improved in NLRP3−/− mice. Taken together, these findings suggest that NLRP3 is a potential therapeutic target for protecting visual cortical neurons against degeneration after ON injury.


NLRP3 Visual cortex Optic nerve injury Visual cortical degeneration 



We would like to thank Prof. Yuan-Guo Zhou from the Army Medical Center of the People’s Liberation Army and Prof. Feng Mei from the Army Medical University (AMU) for project consultation and data evaluation, and thank Prof. Bo Peng from Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, for technical support. This work was supported by the National Natural Science Foundation of China (81570840 and 81200926), the Academician-Led Science and Technological Innovation of Chongqing (cstc2017jcyj-yszxX0006), and the Research Foundation of the Department of Ophthalmology in Daping Hospital, AMU (9-2543).

Conflict of interest

The authors claim that there are no conflicts of interest.

Supplementary material

12264_2019_445_MOESM1_ESM.pdf (790 kb)
Supplementary material 1 (PDF 791 kb)


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Copyright information

© Shanghai Institutes for Biological Sciences, CAS 2019

Authors and Affiliations

  • Zhou Zhang
    • 1
  • Wenyi Liu
    • 1
  • Yubin Huang
    • 2
  • Linlin Luo
    • 1
  • Xiaofeng Cai
    • 1
  • Yunjia Liu
    • 1
  • Liqianyu Ai
    • 1
  • Jun Yan
    • 3
  • Sen Lin
    • 1
    Email author
  • Jian Ye
    • 1
    Email author
  1. 1.Department of Ophthalmology, Research Institute of Surgery and Daping Hospital, Army Medical Center of the People’s Liberation Army (PLA)Army Medical UniversityChongqingChina
  2. 2.Shenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhenChina
  3. 3.Department 1, Research Institute of Surgery and Daping Hospital, Army Medical Center of the PLAArmy Medical UniversityChongqingChina

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