کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10756146 | 1050382 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Alpha-melanocyte stimulating hormone protects retinal pigment epithelium cells from oxidative stress through activation of melanocortin 1 receptor-Akt-mTOR signaling
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کلمات کلیدی
mTORAMDRPEα-MSHMc1rα-Melanocyte stimulating hormone (α-MSH)Hydrogen peroxide - آب اکسیژنهretinal pigment epithelium - اپیتلیوم رنگدانه شبکیهRetinal pigment epithelium (RPE) - اپیتلیوم رنگدانه شبکیه (RPE)age-related macular degeneration - سن تخریب ماکولا مربوط به سن استmammalian target of rapamycin - هدف پستانداران رپامایسینα-Melanocyte stimulating hormone - هورمون تحریک کننده α-ملانوستیH2O2 - هیدروژن پراکسیدMelanocortin 1 receptor - گیرنده ملانوکورتین 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Patients with age related macular degeneration (AMD) will develop vision loss in the center of the visual field. Reactive oxygen species (ROS)-mediated retinal pigment epithelium (RPE) cell apoptosis is an important contributor of AMD. In this study, we explored the pro-survival effect of α-melanocyte stimulating hormone (α-MSH) on oxidative stressed RPE cells. We found that α-MSH receptor melanocortin 1 receptor (MC1R) was functionally expressed in primary and transformed RPE cells. RPE cells were response to α-MSH stimulation. α-MSH activated Akt/mammalian target of rapamycin (mTOR) and Erk1/2 signalings in RPE cells, which were inhibited by MC1R siRNA knockdown. α-MSH protected RPE cells from hydrogen peroxide (H2O2)-induced apoptosis, an effect that was almost abolished when MC1R was depleted by siRNA. α-MSH-mediated S6K1 activation and pro-survival effect against H2O2 was inhibited by Akt inhibitors (perifosine, MK-2206 and LY294002). Further, mTOR inhibition by rapamycin, or by mTOR siRNA knockdown, diminished α-MSH's pro-survival effect in RPE cells. Thus, Akt and its downstream mTOR signaling mediates α-MSH-induced survival in RPE cells. In summary, we have identified a new α-MSH-MC1R physiologic pathway that reduces H2O2-induced RPE cell damage, and might minimize the risk of developing AMD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 443, Issue 2, 10 January 2014, Pages 447-452
Journal: Biochemical and Biophysical Research Communications - Volume 443, Issue 2, 10 January 2014, Pages 447-452
نویسندگان
Li-bo Cheng, Lei Cheng, Hui-e Bi, Zhi-qing Zhang, Jin Yao, Xiao-zhong Zhou, Qin Jiang,