July 2019
Volume 60, Issue 9
Free
ARVO Annual Meeting Abstract  |   July 2019
Ocular pathology elicited by precocious eyelid opening in genetically engineered Prickle 1 knockout mouse model
Author Affiliations & Notes
  • Dianlei Guo
    Zhongshan ophthalmic center, Guangzhou, China
  • Jiali Ru
    Zhongshan ophthalmic center, Guangzhou, China
  • Chunqiao Liu
    Zhongshan ophthalmic center, Guangzhou, China
  • Footnotes
    Commercial Relationships   Dianlei Guo, None; Jiali Ru, None; Chunqiao Liu, None
  • Footnotes
    Support  Guangzhou City Sciences and echnologies Innovation Project (201707020009; Guangzhou, Guangdong Province, China), the National Natural Science Foundation of China (NSFC: 31571077; Beijing, China) and ‘‘100 People Plan’’ from Sun Yat-sen University (8300-18821104; Guangzhou, Guangdong Province, China) to Chunqiao Liu; by grant from Science and Technology Planning Project of Guangdong Province (No. 2015B020226003) to Hong Ouyang
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 4723. doi:
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    • Get Citation

      Dianlei Guo, Jiali Ru, Chunqiao Liu; Ocular pathology elicited by precocious eyelid opening in genetically engineered Prickle 1 knockout mouse model. Invest. Ophthalmol. Vis. Sci. 2019;60(9):4723.

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

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Abstract

Purpose : To investigate the impact of eyelid opening on ocular surface homeostasis, and to present a mouse model for precocious eyelid opening-related keratoconjunctivitis.

Methods : Genetically engineered mouse with ablation of a planar cell polarity gene, Prickle 1, was used for analysis of ocular surface alterations. Wild type and Prickle 1 compound mutant mice with a hypomorphic and a null allele were bred. Whole mount eye ball or H&E stained tissue sections were examined by light microscopy. Cell fate, proliferation, and molecular pathologies were examined by immunohistochemistry. Global mRNA expression profile was obtained by RNAseq using next-generation-sequencing technology. Statistical analysis was performed with Student’s t-test.

Results : Prickle 1 mutant mice showed precocious eyelid reopening and ensuing inflammation of the cornea and conjunctiva accompanied with increased epithelial proliferation, metaplasia of the cornea epithelium, and increased production of goblet cells of conjunctiva. Cornea nerve loss and recovery occurred in phase with the of inflammations. RNAseq and gene ontology analysis revealed molecular changes of the cornea pathology.

Conclusions : A comprehensive ocular surface pathology including cell proliferation, fate transformation and inflammatory cell infiltration associated with precocious eyelid opening in Prickle 1 mutant mice was characterized. The molecular pathological changes in this mouse model might be useful to understand non-infective keratoconjunctivitis triggered by autologous necrotic tissues.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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