| Effects of High Glucose and Dexamethasone on the Permeability in Trabecular Meshwork Cells. |
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Sun Hee Kang, Jae Woo Kim |
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Department of Ophthalmology, Catholic University of Daegu School of Medicine, Daegu, Korea. jwkim@cu.ac.kr |
| 고포도당과 덱사메타존이 섬유주세포의 투과도에 미치는 영향 |
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강선희⋅김재우 |
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대구가톨릭대학교 의과대학 안과학교실 |
Correspondence:
Jae Woo Kim,
Email: jwkim@cu.ac.kr
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Received: 15 June 2017 • Revised: 1 August 2017 • Accepted: 13 February 2018 |
| Abstract |
PURPOSE
To investigate the effects of high glucose (HG) and dexamethasone (DEX) on the survival and permeability of trabecular meshwork cells (HTMC), and associated changes in tight junctions. METHODS: Primary cultured HTMC were exposed to 5 mM low glucose (LG) or 25 mM HG with or without 1.0 µM DEX for 3 days. The permeability of the HTMC monolayer was assessed using carboxyfluorescein or transendothelial electrical resistance (TEER). Gene and protein expressions of claudin-5 and occludin were assessed with reverse transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. RESULTS: HG was significantly associated with greater HTMC monolayer permeability compared to LG by both the carboxyfluorescein permeability test and TEER (p = 0.022, 0.028). HG also decreased claudin-5 and occludin mRNA expression, respectively (7.5%, 12.9%). DEX abolished HG-induced increased permeability, and increased the protein expression of claudin-5 and occludin, respectively (p = 0.015, 0.012). CONCLUSIONS: In HTMCs, DEX reversed HG-induced permeability increase. DEX increased tight junction molecules claudin-5 and occludin. Thus, DEX-induced changes in junctional proteins could be another mechanism of increased resistance through the trabecular meshwork and may result in steroid-induced glaucoma. |
| Key Words:
Dexamethasone;High glucose;Permeability;Tight junction;Trabecular meshwork |
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