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

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

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 2O 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.

Original languageEnglish
Pages (from-to)94-103
Number of pages10
JournalJournal of Pineal Research
Volume51
Issue number1
DOIs
Publication statusPublished - 2011 Aug 1

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Melatonin Receptors
Melatonin
Oxidative Stress
Fibroblasts
Membranes
Glutathione Reductase
Melatonin MT2 Receptor
Paraquat
Corneal dystrophy Avellino type
Catalase
Reactive Oxygen Species
Cell Death
Antioxidants

All Science Journal Classification (ASJC) codes

  • Endocrinology

Cite this

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abstract = "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 2O 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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Melatonin protects against oxidative stress in granular corneal dystrophy type 2 corneal fibroblasts by mechanisms that involve membrane melatonin receptors. / Choi, Seung Il; Dadakhujaev, Shorafidinkhuja; Ryu, Hyunmi; Im Kim, Tae; Kim, Eung Kweon.

In: Journal of Pineal Research, Vol. 51, No. 1, 01.08.2011, p. 94-103.

Research output: Contribution to journalArticle

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