Melatonin Protects Neural Stem Cells Against Tri-Ortho-Cresyl Phosphate-Induced Autophagy

Liu, Chang; Zhou, Wenjuan; Li, Zhaopei; Ren, Jun; Liang, Xian; Li, Shan; Liu, Qian; Song, Fuyong; Hao, Aijun; Wang, Fuwu

doi:10.3389/fnmol.2020.00025

Cited by 5 publications

(3 citation statements)

References 49 publications

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“…Tri-ortho-cresyl phosphate (TOCP) is a material that is widely used in industries. Melatonin protected the mouse E12.5 NSCs from TOCP-induced cell death by suppressing the ROS levels and activating the ERK1/2 signaling pathway [ 108 ] ( Table 10 and Table 11 ).…”

Section: Melatonin and Neurogenesis Impairment Caused By Environmementioning

confidence: 99%

Protective Effects of Melatonin on Neurogenesis Impairment in Neurological Disorders and Its Relevant Molecular Mechanisms

Leung

Cheung

Ngai

et al. 2020

IJMS

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Neurogenesis is the process by which functional new neurons are generated from the neural stem cells (NSCs) or neural progenitor cells (NPCs). Increasing lines of evidence show that neurogenesis impairment is involved in different neurological illnesses, including mood disorders, neurogenerative diseases, and central nervous system (CNS) injuries. Since reversing neurogenesis impairment was found to improve neurological outcomes in the pathological conditions, it is speculated that modulating neurogenesis is a potential therapeutic strategy for neurological diseases. Among different modulators of neurogenesis, melatonin is a particularly interesting one. In traditional understanding, melatonin controls the circadian rhythm and sleep–wake cycle, although it is not directly involved in the proliferation and survival of neurons. In the last decade, it was reported that melatonin plays an important role in the regulation of neurogenesis, and thus it may be a potential treatment for neurogenesis-related disorders. The present review aims to summarize and discuss the recent findings regarding the protective effects of melatonin on the neurogenesis impairment in different neurological conditions. We also address the molecular mechanisms involved in the actions of melatonin in neurogenesis modulation.

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Section: Melatonin and Neurogenesis Impairment Caused By Environmementioning

confidence: 99%

Protective Effects of Melatonin on Neurogenesis Impairment in Neurological Disorders and Its Relevant Molecular Mechanisms

Leung

Cheung

Ngai

et al. 2020

IJMS

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“…As is known, stem cell therapy is considered promising for tissue repair, especially for those with limited regenerative capacities, e.g ., heart and nerve. The seeding cells in myocardial and nerve regeneration, such as mesenchymal stem cells (protection by melatonin has been reported) and neural lineage stem cells (nerve tissues were confirmed to express MR1 also , ), such as neural stem cells and astrocyte precursor cells, may be explored to be modified by MTSNPs in the future. Collectively, the nanoparticles may represent a promising intelligent drug system.…”

Section: Discussionmentioning

confidence: 99%

Mitochondria-Inspired Nanoparticles with Microenvironment-Adapting Capacities for On-Demand Drug Delivery after Ischemic Injury

et al. 2020

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Stimuli-responsive nanoparticles (NPs), so-called "smart" NPs, possess great potentials in drug delivery. Presently, the intelligence of smart NPs is mainly based on their chemical or physical changes to stimuli, which are usually "mechanical" and fundamentally different from biological intelligence. Inspired by mitochondria (MT), a biosmart nanoparticle with microenvironment targeting and self-adaptive capacity (MTSNP) was fabricated for ischemic tissue repair. The nanoparticles were designed as shell@circular DNA@ shell@core. The double shells were like the two-layered membranes of MT, the melatonin-loaded cores corresponded to the MT matrix, and the circular DNA corresponded to MTDNA. In function, melatonin-loaded cores simulated the cell-protective mechanism of MT, which naturally synthesized melatonin to resist ischemia, while circular DNA was constructed to mimic the biological oxygen-sensing mechanism, synthesizing VEGF for vascularization according to oxygen level, like the ATP supply by MT according to microenvironment demand. At the acute stage of ischemia, melatonin was rapidly released from MTSNP to scavenge reactive oxygen species and activated melatonin receptor I on MT to prevent cytochrome c release, which would activate apoptosis. During the chronic stage, circular DNA could sense hypoxia and actively secrete VEGF for revascularization as a response. Importantly, circular DNA could also receive feedback of revascularization and shut down VEGF secretion as an adverse response. Then, the therapeutic potentials of the MTSNP were verified in myocardial ischemia by the multimodality of the methods. Such nanoparticles may represent a promising intelligent nanodrug system.

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“…For instance, a number of studies has dealt with adjunctive roles of melatonin for the success of transplantation or injection of stem cells at injured or dysfunctional sites [10][11][12][13][14][15][16][17][18]. Similarly, the antioxidant and anti-inflammatory properties of melatonin have been taken as a reason for protecting stem cells against oxidative and inflammatory insults [13,15,[19][20][21][22][23][24][25][26][27]. Although this information is of high value, it largely exceeds the topic of stem cell programming.…”

Section: Introductionmentioning

confidence: 99%

Melatonin and the Programming of Stem Cells

Hardeland

2022

IJMS

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Melatonin interacts with various types of stem cells, in multiple ways that comprise stimulation of proliferation, maintenance of stemness and self-renewal, protection of survival, and programming toward functionally different cell lineages. These various properties are frequently intertwined but may not be always jointly present. Melatonin typically stimulates proliferation and transition to the mature cell type. For all sufficiently studied stem or progenitor cells, melatonin’s signaling pathways leading to expression of respective morphogenetic factors are discussed. The focus of this article will be laid on the aspect of programming, particularly in pluripotent cells. This is especially but not exclusively the case in neural stem cells (NSCs) and mesenchymal stem cells (MSCs). Concerning developmental bifurcations, decisions are not exclusively made by melatonin alone. In MSCs, melatonin promotes adipogenesis in a Wnt (Wingless-Integration-1)-independent mode, but chondrogenesis and osteogenesis Wnt-dependently. Melatonin upregulates Wnt, but not in the adipogenic lineage. This decision seems to depend on microenvironment and epigenetic memory. The decision for chondrogenesis instead of osteogenesis, both being Wnt-dependent, seems to involve fibroblast growth factor receptor 3. Stem cell-specific differences in melatonin and Wnt receptors, and contributions of transcription factors and noncoding RNAs are outlined, as well as possibilities and the medical importance of re-programming for transdifferentiation.

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Melatonin Protects Neural Stem Cells Against Tri-Ortho-Cresyl Phosphate-Induced Autophagy

Cited by 5 publications

References 49 publications

Protective Effects of Melatonin on Neurogenesis Impairment in Neurological Disorders and Its Relevant Molecular Mechanisms

Protective Effects of Melatonin on Neurogenesis Impairment in Neurological Disorders and Its Relevant Molecular Mechanisms

Mitochondria-Inspired Nanoparticles with Microenvironment-Adapting Capacities for On-Demand Drug Delivery after Ischemic Injury

Melatonin and the Programming of Stem Cells

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