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Melatonin antagonizes oxidative stress-induced mitochondrial dysfunction in retinal pigmented epithelium cells via melatonin receptor 1 (MT1).
J Toxicol Sci. 2018; 43(11):659-669.JT

Abstract

High energy-consumption in retinal pigmented epithelium (RPE) cells poses oxidative stress (OS) and contributes to mitochondrial dysfunction (MD) for retinal degeneration-associated diseases. In the present study, we evaluated the protective role of Melatonin, a natural antioxidant, against the hydrogen peroxide (H2O2)-induced damage to RPE cells. The cellular viability, apoptosis, the expression of apoptosis-associated proteins and mitochondrial function were examined in the retinal ARPE-19 cells, post the treatment with H2O2 or (and) with Melatonin. The regulation by Melatonin receptor 1 (MT1) on the Melatonin-mediated protection was also examined via MT1 knockdown with siRNA. Results demonstrated that Melatonin significantly ameliorated cell viability reduction, reduced apoptosis and downregulated the apoptosis-associated proteins in H2O2-treated ARPE-19 cells. The H2O2-induced mitochondrial dysfunction was also significantly blocked by the Melatonin treatment, presenting as a reduced accumulation of reactive oxygen species (ROS) and mitochondrial superoxide and an ameliorated reduction of mitochondrial membrane potential (MMP). In addition, the knockdown of MT1 with MT1-specific siRNA inhibited the Melatonin-mediated protection against OS damage in ARPE-19 cells. In summary, we confirmed the protective role of Melatonin against H2O2-induced mitochondrial dysfunction in RPE cells. MT1 knockdown blocked such protective role of Melatonin. It is implied that Melatonin exerts a protective role against oxidative stress via Melatonin-MT1 signaling in RPE cells.

Authors+Show Affiliations

Department of Ophthalmology, The Affiliated Yantai Yuhuangding Hospital of Medical College, Qingdao University, China.Department of Physical Examination, The Affiliated Yantai Yuhuangding Hospital of Medical College, Qingdao University, China.Department of Ophthalmology, Laiyang Central Hospital, China.Depertment of Ophthalmology, Linyi People's Hospital, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30404999

Citation

Yan, Guigang, et al. "Melatonin Antagonizes Oxidative Stress-induced Mitochondrial Dysfunction in Retinal Pigmented Epithelium Cells Via Melatonin Receptor 1 (MT1)." The Journal of Toxicological Sciences, vol. 43, no. 11, 2018, pp. 659-669.
Yan G, Yu L, Jiang S, et al. Melatonin antagonizes oxidative stress-induced mitochondrial dysfunction in retinal pigmented epithelium cells via melatonin receptor 1 (MT1). J Toxicol Sci. 2018;43(11):659-669.
Yan, G., Yu, L., Jiang, S., & Zhu, J. (2018). Melatonin antagonizes oxidative stress-induced mitochondrial dysfunction in retinal pigmented epithelium cells via melatonin receptor 1 (MT1). The Journal of Toxicological Sciences, 43(11), 659-669. https://doi.org/10.2131/jts.43.659
Yan G, et al. Melatonin Antagonizes Oxidative Stress-induced Mitochondrial Dysfunction in Retinal Pigmented Epithelium Cells Via Melatonin Receptor 1 (MT1). J Toxicol Sci. 2018;43(11):659-669. PubMed PMID: 30404999.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Melatonin antagonizes oxidative stress-induced mitochondrial dysfunction in retinal pigmented epithelium cells via melatonin receptor 1 (MT1). AU - Yan,Guigang, AU - Yu,Lianzhi, AU - Jiang,Songmei, AU - Zhu,Jianfeng, PY - 2018/11/9/entrez PY - 2018/11/9/pubmed PY - 2018/11/27/medline KW - Melatonin KW - Mitochondrial dysfunction (MD) KW - Oxidative stress (OS) KW - Retinal pigmented epithelium (RPE) cells SP - 659 EP - 669 JF - The Journal of toxicological sciences JO - J Toxicol Sci VL - 43 IS - 11 N2 - High energy-consumption in retinal pigmented epithelium (RPE) cells poses oxidative stress (OS) and contributes to mitochondrial dysfunction (MD) for retinal degeneration-associated diseases. In the present study, we evaluated the protective role of Melatonin, a natural antioxidant, against the hydrogen peroxide (H2O2)-induced damage to RPE cells. The cellular viability, apoptosis, the expression of apoptosis-associated proteins and mitochondrial function were examined in the retinal ARPE-19 cells, post the treatment with H2O2 or (and) with Melatonin. The regulation by Melatonin receptor 1 (MT1) on the Melatonin-mediated protection was also examined via MT1 knockdown with siRNA. Results demonstrated that Melatonin significantly ameliorated cell viability reduction, reduced apoptosis and downregulated the apoptosis-associated proteins in H2O2-treated ARPE-19 cells. The H2O2-induced mitochondrial dysfunction was also significantly blocked by the Melatonin treatment, presenting as a reduced accumulation of reactive oxygen species (ROS) and mitochondrial superoxide and an ameliorated reduction of mitochondrial membrane potential (MMP). In addition, the knockdown of MT1 with MT1-specific siRNA inhibited the Melatonin-mediated protection against OS damage in ARPE-19 cells. In summary, we confirmed the protective role of Melatonin against H2O2-induced mitochondrial dysfunction in RPE cells. MT1 knockdown blocked such protective role of Melatonin. It is implied that Melatonin exerts a protective role against oxidative stress via Melatonin-MT1 signaling in RPE cells. SN - 1880-3989 UR - https://www.unboundmedicine.com/medline/citation/30404999/Melatonin_antagonizes_oxidative_stress_induced_mitochondrial_dysfunction_in_retinal_pigmented_epithelium_cells_via_melatonin_receptor_1__MT1__ L2 - https://dx.doi.org/10.2131/jts.43.659 DB - PRIME DP - Unbound Medicine ER -