Loss of aquaporin 5 contributes to the corneal epithelial pathogenesis via Wnt/β‐catenin pathway

Author:

Wang Yihui1,Di Guohu12ORCID,Zhang Kaier1,Bai Ying1,Cao Xin1,Zhao Hui3,Wang Dianqiang4,Chen Peng12ORCID

Affiliation:

1. Department of Human Anatomy, Histology and Embryology School of Basic Medicine, Qingdao University Qingdao China

2. Institute of Stem Cell Regeneration Medicine, School of Basic Medicine Qingdao University Qingdao China

3. The 971 Hospital of the Chinese People's Liberation Army Navy Qingdao China

4. Department of Ophthalmology Qingdao Aier Eye Hospital Qingdao China

Abstract

AbstractAQP5 plays a crucial role in maintaining corneal transparency and the barrier function of the cornea. Here, we found that in the corneas of Aqp5−/− mice at older than 6 months, loss of AQP5 significantly increased corneal neovascularization, inflammatory cell infiltration, and corneal haze. The results of immunofluorescence staining showed that upregulation of K1, K10, and K14, and downregulation of K12 and Pax6 were detected in Aqp5−/− cornea and primary corneal epithelial cells. Loss of AQP5 aggravated wound‐induced corneal neovascularization, inflammation, and haze. mRNA sequencing, western blotting, and qRT‐PCR showed that Wnt2 and Wnt6 were significantly decreased in Aqp5−/− corneas and primary corneal epithelial cells, accompanied by decreased aggregation in the cytoplasm and nucleus of β‐catenin. IIIC3 significantly suppressed corneal neovascularization, inflammation, haze, and maintained corneal transparent epithelial in Aqp5−/− corneas. We also found that pre‐stimulated Aqp5−/− primary corneal epithelial cells with IIIC3 caused the decreased expression of K1, K10, and K14, the increased expression of K12, Pax6, and increased aggregation in the cytoplasm and nucleus of β‐catenin. These findings revealed that AQP5 may regulate corneal epithelial homeostasis and function through the Wnt/β‐catenin signaling pathway. Together, we uncovered a possible role of AQP5 in determining corneal epithelial cell fate and providing a potential therapeutic target for corneal epithelial dysfunction.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Shandong Province

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

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