Role of phosphatidylinositol 3 kinase pathway in corneal damage due to blue light exposure Cornea BlueLight PI3K AKT Ccorneal Epithelial Apoptosis ReactiveOxygenSpecies Autophagy ResearchSquare
By Pooja Toshniwal PahariaMar 1 2023Reviewed by Benedette Cuffari, M.Sc. *Important notice: Research Square publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Exposure to blue light can alleviate epithelial-mesenchymal conversion through impaired cellular autophagy, activation of the nuclear factor kappa B pathway, and induce ocular dryness. However, whether the PI3K/AKT pathway is involved in the pathophysiology of damage is not clear. To investigate the role of the PI3K/AKT pathway, hCECs were treated with LY294002, an inhibitor of the AKT pathway. Zona occludens 1 , N-cadherin , and E-cadherin expression was assessed and the E-cadherin/N-cadherin ratio was calculated.
In comparison to the zero-hour dimethyl sulfoxide -treated hCECs, p-p70S6K/p70S6K and p-AKT/AKT ratios were markedly reduced in the zero-hour LY294002, two-day DMSO, and two-day LY294002 treatment groups. This similarly demonstrated PI3K/AKT/p70S6K inhibition among blue light-exposed hCECs. The scratch assay findings indicated delayed wound healing among LY294002-treated hCECs and those exposed to blue light for two days. Among the zero-hour LY294002-treated, two-day DMSO-treated, and two-day LY294002-treated hCECs, ZO-1 and E-cad levels were significantly elevated, whereas N-cad levels were markedly lowered as compared to the zero-hour DMSO-treated group.
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