NDLI: Inhibition of mTOR signaling protects photoreceptor cells against serum deprivation by reducing oxidative stress and inducing G2/M cell cycle arrest.

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Inhibition of mTOR signaling protects photoreceptor cells against serum deprivation by reducing oxidative stress and inducing G2/M cell cycle arrest.

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Inhibition of mTOR signaling protects photoreceptor cells against serum deprivation by reducing oxidative stress and inducing G2/M cell cycle arrest.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Song, Jing-Yao Li, Guang-Yu Li, Fu-Qaing Chen, Xu Fan, Bin
Description	Author Affiliation: Fan B ( Department of Ophthalmology, Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.); Li FQ ( Department of Ophthalmology, Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.); Song JY ( Department of Ophthalmology, Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.); Chen X ( Department of Ophthalmology, Zhongshan Hospital of Fudan University, Shanghai 200032, P.R. China.); Li GY ( Department of Ophthalmology, Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.)
Abstract	The mammalian target of rapamycin (mTOR) pathway is a crucial cellular signaling hub, which integrates internal and external cues to modulate the cell cycle, protein synthesis and metabolism. The present study hypothesized that inhibiting mTOR signaling may induce cells to enter lower and more stable bioenergetic states, in which neurons have greater resistance to various insults. Neurotrophin withdrawal from photoreceptor cells (661W cells) was mimicked using serum deprivation, and the neuroprotective mechanisms were studied following suppression of the mTOR pathway. Treatment with an mTOR specific inhibitor, rapamycin, reduced intracellular levels of reactive oxygen species, suppressed oxidative stress, and attenuated mitochondrial dysfunction. In addition, inhibiting mTOR signaling induced a G2/M cell cycle arrest, thus providing an opportunity to repair damaged DNA and block the cell death cascade. These results suggested that inhibition of mTOR had a neuroprotective effect on serumdeprived 661W cells. In conclusion, the mTOR pathway is a critical molecular signal for cell cycle regulation and energy metabolism, and inhibiting the mTOR pathway may attenuate neurotrophin withdrawalinduced damage. These observations may provide evidence for the treatment of retinal degenerative disease, since inducing neurons into a lower and more stable bioenergetic state by blocking mTOR signaling may slow the progression of neurodegenerative diseases.
ISSN	17912997
e-ISSN	17913004
DOI	10.3892/mmr.2016.5011
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	13
Language	English
Publisher	Spandidos Publications
Publisher Date	2016-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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