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Open AccessArticle

Melatonin Suppresses Autophagy Induced by Clinostat in Preosteoblast MC3T3-E1 Cells

1
Yonsei-Fraunhofer Medical Device Laboratory, Department of Biomedical Engineering, Yonsei University, Wonju, 26493 Gangwon-do, Korea
2
Fraunhofer Institute IKTS-MD, Maria-Reiche-Str.2, 01109 Dresden, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Irmgard Tegeder
Int. J. Mol. Sci. 2016, 17(4), 526; https://doi.org/10.3390/ijms17040526
Received: 2 March 2016 / Revised: 25 March 2016 / Accepted: 5 April 2016 / Published: 8 April 2016
(This article belongs to the Section Biochemistry)
Microgravity exposure can cause cardiovascular and immune disorders, muscle atrophy, osteoporosis, and loss of blood and plasma volume. A clinostat device is an effective ground-based tool for simulating microgravity. This study investigated how melatonin suppresses autophagy caused by simulated microgravity in preosteoblast MC3T3-E1 cells. In preosteoblast MC3T3-E1 cells, clinostat rotation induced a significant time-dependent increase in the levels of the autophagosomal marker microtubule-associated protein light chain (LC3), suggesting that autophagy is induced by clinostat rotation in these cells. Melatonin treatment (100, 200 nM) significantly attenuated the clinostat-induced increases in LC3 II protein, and immunofluorescence staining revealed decreased levels of both LC3 and lysosomal-associated membrane protein 2 (Lamp2), indicating a decrease in autophagosomes. The levels of phosphorylation of mammalian target of rapamycin (p-mTOR) (Ser2448), phosphorylation of extracellular signal-regulated kinase (p-ERK), and phosphorylation of serine-threonine protein kinase (p-Akt) (Ser473) were significantly reduced by clinostat rotation. However, their expression levels were significantly recovered by melatonin treatment. Also, expression of the Bcl-2, truncated Bid, Cu/Zn- superoxide dismutase (SOD), and Mn-SOD proteins were significantly increased by melatonin treatment, whereas levels of Bax and catalase were decreased. The endoplasmic reticulum (ER) stress marker GRP78/BiP, IRE1α, and p-PERK proteins were significantly reduced by melatonin treatment. Treatment with the competitive melatonin receptor antagonist luzindole blocked melatonin-induced decreases in LC3 II levels. These results demonstrate that melatonin suppresses clinostat-induced autophagy through increasing the phosphorylation of the ERK/Akt/mTOR proteins. Consequently, melatonin appears to be a potential therapeutic agent for regulating microgravity-related bone loss or osteoporosis. View Full-Text
Keywords: melatonin; autophagy; ERK; Akt; mTOR; clinostat; MC3T3-E1 cells melatonin; autophagy; ERK; Akt; mTOR; clinostat; MC3T3-E1 cells
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MDPI and ACS Style

Yoo, Y.-M.; Han, T.-Y.; Kim, H.S. Melatonin Suppresses Autophagy Induced by Clinostat in Preosteoblast MC3T3-E1 Cells. Int. J. Mol. Sci. 2016, 17, 526. https://doi.org/10.3390/ijms17040526

AMA Style

Yoo Y-M, Han T-Y, Kim HS. Melatonin Suppresses Autophagy Induced by Clinostat in Preosteoblast MC3T3-E1 Cells. International Journal of Molecular Sciences. 2016; 17(4):526. https://doi.org/10.3390/ijms17040526

Chicago/Turabian Style

Yoo, Yeong-Min; Han, Tae-Young; Kim, Han S. 2016. "Melatonin Suppresses Autophagy Induced by Clinostat in Preosteoblast MC3T3-E1 Cells" Int. J. Mol. Sci. 17, no. 4: 526. https://doi.org/10.3390/ijms17040526

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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