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Melatonin protects against oxidative stress in granular corneal dystrophy type 2 corneal fibroblasts by mechanisms that involve membrane melatonin receptors

 Seung-Il Choi  ;  Shorafidinkhuja Dadakhujaev  ;  Hyunmi Ryu  ;  Tae im Kim  ;  Eung Kweon Kim 
 JOURNAL OF PINEAL RESEARCH, Vol.51(1) : 94-103, 2011 
Journal Title
Issue Date
Analysis of Variance ; Antioxidants/pharmacology ; Blotting, Western ; Catalase/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cornea/drug effects ; Cornea/pathology ; Corneal Dystrophies, Hereditary/drug therapy* ; Corneal Dystrophies, Hereditary/metabolism* ; Corneal Dystrophies, Hereditary/pathology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Flow Cytometry ; Glutathione Reductase/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Immunohistochemistry ; Melatonin/pharmacology* ; Oxidative Stress/drug effects* ; Paraquat/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Melatonin/metabolism* ; Superoxide Dismutase/metabolism
corneal fibroblasts ; granular corneal dystrophy type 2 ; melatonin ; melatonin receptors ; oxidative stress
Considering that oxidative stress plays a role in corneal fibroblast degeneration during granular corneal dystrophy type 2 (GCD2) and melatonin is an effective antioxidant, we examined the ability of melatonin to protect against oxidative stress-induced cell death of primary cultured normal and GCD2-homozygous corneal fibroblasts. Melatonin treatment protected primary cultured normal and GCD2 corneal fibroblasts from paraquat (PQ)-induced oxidative stress and caused increased expression levels of Cu/Zn-superoxide dismutase (SOD1) and glutathione reductase (GR) in both types of cells. Interestingly, catalase expression increased in normal corneal fibroblasts, but decreased in GCD2 corneal fibroblasts after melatonin treatment. Melatonin also reduced the levels of intracellular reactive oxygen species and H(2)O(2) in both cell types. In addition, the selective melatonin receptor antagonist luzindole blocked melatonin-induced expression of SOD1 and GR. The expression levels of melatonin receptors 1A (MT1) and 1B (MT2) were significantly higher in GCD2 corneal fibroblasts than in normal cells. These results suggest that increased expression of melatonin receptors may be involved in the defense mechanisms against oxidative stress in GCD2 corneal fibroblasts, and melatonin may have potential therapeutic implications for GCD2 treatment.
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Appears in Collections:
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Eung Kweon(김응권) ORCID logo https://orcid.org/0000-0002-1453-8042
Kim, Tae Im(김태임) ORCID logo https://orcid.org/0000-0001-6414-3842
Dadakhujaev, Shorafidinkhuja(다다후자예프)
Ryu, Hyun Mi(류현미)
Choi, Seung Il(최승일) ORCID logo https://orcid.org/0000-0001-7168-8795
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