Effects of High Glucose and Dexamethasone on the Permeability in Trabecular Meshwork Cells
10.3341/jkos.2018.59.3.252
- Author:
Sun Hee KANG
1
;
Jae Woo KIM
Author Information
1. Department of Ophthalmology, Catholic University of Daegu School of Medicine, Daegu, Korea. jwkim@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Dexamethasone;
High glucose;
Permeability;
Tight junction;
Trabecular meshwork
- MeSH:
Blotting, Western;
Claudin-5;
Dexamethasone;
Electric Impedance;
Glaucoma;
Glucose;
Occludin;
Permeability;
Polymerase Chain Reaction;
Reverse Transcription;
RNA, Messenger;
Tight Junctions;
Trabecular Meshwork
- From:Journal of the Korean Ophthalmological Society
2018;59(3):252-260
- CountryRepublic of Korea
- Language:Korean
-
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.
