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Satoshi Iwamoto, Tomoaki Koga, Toshiaki Okuno, Akira Murakami, Akira Matsuda, Takehiko Yokomizo; NSAIDs causes corneal epithelial damage by inhibition of leukotriene B4 receptor 2 signaling. Invest. Ophthalmol. Vis. Sci. 2016;57(12):1252.
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© ARVO (1962-2015); The Authors (2016-present)
Compromised corneal epithelialization in patients treated with NSAIDs had been reported. However, pathophysiological mechanism of delayed corneal wound healing with non-steroidal anti-inflammatory drugs (NSAIDs) usage is still not clear. In ARVO 2015, we reported that a non-canonical BLT2(Leukotriene B4 receptor 2) ligand, 12(S)-hydroxyheptadecatrienoic acid (12-HHT) accelerated corneal epithelial wound healing, and 12-HHT production is inhibited by NSAIDs eye drop. In this study, we further investigated the mechanism how 12-HHT/BLT2 pathway accelerate corneal epithelialization.
Naïve corneal tissue obtained from BLT2(-/-) and congenic wild type (WT) mice was subjected to next generation sequencing (NGS) analysis to compare gene expression profiles. Human corneal epithelial cell line (HCET) overexpressed BLT2 gene was established and scratch assay experiments were carried out.
The expression of acta2 gene (encoding alpha-smooth muscle actin) was attenuated in the naïve cornea of BLT(-/-) mouse compared to WT mouse. In BLT2 overexpressed HCET cells, accelerated epithelial cell wound closure and increase of acta2 gene expression was observed.
12-HHT/BLT2 pathway accelerates corneal epithelial wound healing with increase of acta2 gene expression.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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