Purchase this article with an account.
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.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate the impact of eyelid opening on ocular surface homeostasis, and to present a mouse model for precocious eyelid opening-related keratoconjunctivitis.
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.
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.
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.
This PDF is available to Subscribers Only