Ocular surface pathogenesis associated with precocious eyelid opening and necrotic autologous tissue in mouse with disruption of Prickle 1 gene
Related Experiment Video
Updated: Jan 31, 2026
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
Published on: August 4, 2022
Dianlei Guo1, Mengke Li1, Bin Zou1
1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, 54 Xianlie South Road, Guangzhou 510060, China.
Abstract:
Ocular surface disease is one major type of eye diseases. Different etiologies trigger distinct pathological responses of the ocular surface. We previously reported that genetically engineered mice with ablation of Prickle 1 manifested precocious eyelid opening with ensuing cornea dysplasia. The current study aimed to characterize the molecular traits and the direct cause of ocular pathology associated with precocious eyelid opening in the Prickle 1 mutant mouse. Prickle 1 mutant mice exhibited a slew of ocular surface pathology including cell proliferation, cell fate transformation and inflammatory infiltration coinciding with the timing of the precocious eyelid opening. Forced eyelid opening in wild type mice did not induce cornea pathology comparable to that of the Prickle 1 mutants. Necrotic tissue debris was found associated with the lesioned cornea. RNAseq analysis of the mutant cornea revealed an expression profile shared by a range of dermatological diseases involving immune responses and cancer. Taken together, the data suggest that the necrotic eyelid debris plays an important role in ocular pathogenesis of the Prickle 1 mutant mouse, which may represent a type of non-infectious keratoconjunctivitis caused by damaged autologous tissues. Additionally, Prickle 1 mutant cornea pathogenesis may offer molecular insights into other types of epithelial pathogenesis.
Insights
Prickle 1 mutant mice show precocious eyelid opening, leading to ocular surface disease. Necrotic eyelid debris causes this keratoconjunctivitis, offering insights into epithelial pathogenesis.
Area of Science:
- Ophthalmology
- Developmental Biology
- Immunology
Background:
- Ocular surface disease encompasses various eye conditions with diverse causes.
- Previous research identified Prickle 1 gene ablation in mice leading to premature eyelid opening and corneal abnormalities.
Purpose of the Study:
- To investigate the molecular mechanisms behind ocular pathology in Prickle 1 mutant mice with precocious eyelid opening.
- To determine the direct cause of corneal damage in these mutants.
Main Methods:
- Comparative analysis of Prickle 1 mutant mice and wild-type mice with experimentally induced eyelid opening.
- Histopathological examination of ocular surface tissues.
- RNA sequencing (RNAseq) analysis of mutant corneas.
Main Results:
- Prickle 1 mutants displayed ocular surface pathology, including cell proliferation, altered cell fate, and inflammation, concurrent with premature eyelid opening.
- Forced eyelid opening in wild-type mice did not replicate the corneal pathology seen in mutants.
- RNAseq revealed gene expression profiles in mutant corneas associated with immune responses and cancer, similar to dermatological diseases.
- Necrotic eyelid debris was identified as a key factor in the corneal lesions.
Conclusions:
- The ocular pathology in Prickle 1 mutant mice is likely caused by necrotic eyelid debris, suggesting a form of non-infectious keratoconjunctivitis due to autologous tissue damage.
- The study provides molecular insights into epithelial pathogenesis, potentially applicable to other conditions.
- Prickle 1 plays a critical role in maintaining ocular surface integrity during development.
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