| Effect of Rho Kinase Inhibitor on the Production of Nitric Oxide in Trabecular Meshwork Cells. |
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Jae Woo Kim, Keun Hae Kim, Seok Jin Hwang |
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Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea. jwkim@cu.ac.kr |
| 섬유주세포에서 Rho Kinase 저해제가 일산화질소의 생성에 미치는 영향 |
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김재우⋅김근해⋅황석진 |
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대구가톨릭대학교 의과대학 안과학교실 |
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Correspondence:
Jae Woo Kim |
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Received: 17 December 2015 • Revised: 15 January 2016 • Accepted: 25 February 2016 |
| Abstract |
PURPOSE
To investigate the effects of Rho kinase (ROCK) inhibitor on the production of nitric oxide (NO) and expression of endothelial nitric oxide synthase (eNOS) in cultured human trabecular meshwork cells (HTMC). METHODS: Primarily cultured HTMC were exposed to 0 µM, 10 µM or 100 µM Y-27632 for 3 days and NO production was assessed using Griess assay. After 24 hours, the effect of Y-27632 on the contraction of collagen matrix and the permeability of the HTMC monolayer was determined. The expression of eNOS mRNA was assessed using reverse transcription-polymerase chain reaction (RT-PCR) and cellular survival with the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. RESULTS: In HTMC, 10 µM and 100 µM Y-27632 significantly increased NO production after 1 day and 3 days (p = 0.020 and 0.001, respectively). At 1 day after exposure, Y-276320 significantly relaxed the collagen matrix and increased the permeability of the HTMC monolayer (all p = 0.001) and the eNOS mRNA expression (p = 0.039). CONCLUSIONS: Increased NO production may play a role in the mechanism of increased trabecular outflow associated with ROCK inhibitor. |
| Key Words:
Endothelial nitric oxide synthase (eNOS);Nitric oxide;Rho kinase (ROCK) inhibitor;Trabecular meshwork;Y-276320 |
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