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Qinxiang Zheng, Huihui Lu, Wei Chen; AQP5 Promotes Inflammation and Apoptosis via JNK Activation in Hyperosmolarity Stressed Human Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2017;58(8):801.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the role of water channel Aquaporin5 (AQP5) and JNK pathway in hyperosmolarity-induced inflammation and cell apoptosis in human corneal epithelial cells (HCECs), and evaluate the relationship of AQP5, JNK, and the proinflammatory cytokines involved in dry eye (DE) progression.
Immortalized HCECs were cultured in different hyperosmolarities (450, 500 and 550 mOsm), and their mRNA levels of IL-1β, IL-6, IL-8, TNF-α, apoptosis factor caspase-1, and AQP5 were compared with those of the isosmotic group, as well as the protein levels of AQP5 and p-JNK. Then HCECs cultured in 310 mOsm media were switched to 500 mOsm media, with or without the pretreatment of an p-JNK inhibitor SP600125. Also the HCECs transfected with interference RNA targeted at AQP5 or negative control (NC) gene were cultivated in 500 mOsm media. The expressions of the same cytokines and the level of cell apoptosis were evaluated.
The mRNA levels of IL-1β, IL-6, IL-8, TNF-α, caspase-1, and AQP5 increased in hyperosmotic media above 500 mOsm, with the protein levels of AQP5 and p-JNK elevated (P ≤ 0.019). The pre-treatment of 20μM SP600125 reduced the mRNA levels of the same cytokines, the translational levels of AQP5 and p-JNK, as well as the cell apoptotic level (P ≤ 0.015). SiAQP5 transfection effectively downregulated the transcriptional levels of these cytokines and cell apoptosis (P ≤ 0.016).
AQP5 was involved in the promotion of hyperosmolarity-induced inflammation and cell apoptosis in HCECs, which might be regulated by the p-JNK activity. The water channel proteins might play a critical role in DE progression.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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