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자료유형
학술저널
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저널정보
대한안과학회 Korean Journal of Ophthalmology Korean Journal of Ophthalmology 제34권 제2호
발행연도
2020.1
수록면
97 - 105 (9page)

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Purpose: To investigate the pathway and effects of minoxidil on trabecular outflow in cultured human trabecularmeshwork (TM) cells. Methods: After exposing primarily cultured TM cells to 0, 10, 50, or 100 μM minoxidil sulfate (MS), trabecularoutflow was assessed by measuring TM cell monolayer permeability to carboxyfluorescein and transepithelialelectrical resistance. To assess the pathway of permeability changes, caveolin-1, occludin, and claudin-5levels were measured via western blot. Generation of reactive oxygen species (ROS) was measured usingthe dichlorofluorescein diacetate assay. To assess the involvement of nitric oxide (NO) in minoxidil-inducedpermeability increase, the degrees of endothelial nitric oxide synthase mRNA expression and NO productionwere measured with reverse transcription polymerase chain reaction and Griess assays, respectively. Permeabilitywas also measured with co-exposure to 50 μM N-acetyl cysteine. Results: MS significantly increased TM cell monolayer permeability (p < 0.05) and decreased transepithelialelectrical resistance (p < 0.05). MS decreased the degree of endothelial nitric oxide synthase mRNA expressionbut did not affect NO production. MS decreased occludin and claudin-5 levels but did not affect caveolin-1level. MS at 100 μM increased the generation of ROS, and MS-induced permeability increase was attenuatedafter co-exposure to 50 μM N-acetyl cysteine. Conclusions: Minoxidil may preferentially increase trabecular permeability via a paracellular pathway by downregulationof tight junction proteins. This minoxidil-induced permeability through the TM may be mediated bygeneration of ROS.

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