Melatonin promotes proliferation of neural stem cells from adult mouse spinal cord <i>via</i> the PI3K/AKT signaling pathway

Yu, Shuntai; Zhang, Xuefeng; Xu, Zilan; Hu, Changlong

doi:10.1002/1873-3468.13458

Cited by 17 publications

(12 citation statements)

References 35 publications

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“…The most frequently observed signal transmission is that of the canonical ERK/MAPK pathway [19,107,[114][115][116]. Another repeatedly reported downstream pathway is that of PI3K/AKT signaling [20,27,88,112,117]. These findings are in line with those on programming of other stem cells, especially MSCs, as will be discussed in Section 8.…”

Section: Neurogenesis From Nscs/nspcssupporting

confidence: 65%

“…These observations are in accordance with the multiple results on NSC protection, proliferation, and differentiation both in vivo and in vitro (Table 1). Rat midbrain NSCs None Viability↑ dopaminergic differentiation (tyrosine hydroxylase↑), BDNF↑ GDNF↑ [110] Mouse NSCs from ganglionic eminence None Differentiation to neurons↑ in FBS-stimulated proliferation, but not in differentiation period [111] Murine induced pluripotent stem cells None Differentiation to NSCs↑ and further to neurons↑ PI3K/AKT signaling [112] Mouse hippocampal NSCs None Survival↑ differentiation↑ [113] NSCs from adult murine SVZ None Proliferation↑ differentiation↑; ERK/MAPK signaling [114,115] Rat adult hippocampal NSCs None Proliferation↑ phosphorylation of ERK1/2 andc-Raf [116] Mouse adult spinal cord NSPCs None Proliferation↑ PI3K/AKT signaling [117] Murine hippocampus in vivo None Neurogenesis↑ [118] Murine dentate gyrus in vivo None NeuN+ cells↑ DCX+ cells↑ [108,113,[119][120][121][122][123][124] Rat dentate gyrus in vivo Pinealectomy Neurogenesis↑ [125] Rat embryonal NSCs IL-18 Proliferation↑ differentiation↑ BDNF↑ GDNF↑ [126] Mouse embryonic cortical NSCs LPS Sox2 expression↑ PI3K/Akt/Nrf2 signaling [20] Mouse cortical NSCs in vitro Hypoxia Proliferation↑ differentiation to neurons↑ MT 1 dependence, pERK1/2↑ [19] Mouse embryonic cortical NSCs Hyperglycemia Proliferation↑ self-renewal↑ autophagy↓ [127] Murine dentate gyrus in vivo Corticosterone Attenuation of proliferation suppression [128] Rat adult hippocampal NSCs Dexamethasone Reversal of inhibition of nestin and Ki67 expression [129] Murine dentate gyrus in vivo Dexamethasone Attenuation of suppressed DCX expression [130] Murine dentate gyrus in vivo Cuprizone Restoration of Ki67+ proliferative cells and DCX+ NPCs; BNDF↑ [131] Murine dentate gyrus in vivo Scopolamine Restoration of Ki67+ proliferative cells and DCX+ NPCs [132] Murine dentate gyrus in vivo d-Galactose (aging model) Restoration of Ki67+ proliferative cells and DCX+ NPCs…”

Section: Neurogenesis From Nscs/nspcsmentioning

confidence: 99%

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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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Section: Neurogenesis From Nscs/nspcssupporting

confidence: 65%

Section: Neurogenesis From Nscs/nspcsmentioning

confidence: 99%

Melatonin and the Programming of Stem Cells

Hardeland

2022

IJMS

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“…When mice were subjected to 10 mg/kg luzindole daily for 14 days, DCX+ neuronal precursor cells and Ki-67+ proliferative cells in the subgranular zone (SGZ) reduced [ 45 ]. Ex vivo studies also showed that melatonin increased survival, proliferation, and differentiation of adult SVZ, hippocampal, and spinal cord NSCs through the melatonin receptors via the ERK/MAPK and PI3K/Akt signaling pathways [ 33 , 34 , 35 , 36 , 37 ] ( Table 1 and Table 2 ).…”

Section: Roles Of Melatonin In Modulation Of Neurogenesismentioning

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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“…Furthermore, melatonin enhanced in vitro proliferation of neural stem cells from adult mouse spinal cord via the participation of receptors and the PI3K/Akt pathway (Yu et al, 2019). In this sense, our findings suggest that the interaction of melatonin with the MT 1 receptor and further activation of the PI3K/Akt/FOXO3a pathway is potentially involved in the maintenance of survival and stimulation of primordial follicle activation in vitro in sheep.…”

Section: Discussionmentioning

confidence: 55%

Immunolocalization of melatonin receptor type 1 in the sheep ovary and involvement of the PI3K/Akt/FOXO3a signaling pathway in the effects of melatonin on survival and in vitro activation of primordial follicles

Barberino

Macedo

Lins

et al. 2022

Molecular Reproduction Devel

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This study characterized the expression of melatonin receptor type 1 (MT 1 ) protein in sheep ovaries, evaluated melatonin effects on primordial follicle survival and development after in vitro culture of ovarian tissue and verified the possible involvement of the phosphatidylinositol-3-kinase/protein kinase B/forkhead box O3a (PI3K/Akt/FOXO3a) pathway in the melatonin actions. Ovine ovarian fragments were cultured in α-modified minimum essential medium alone (α-MEM + ) or supplemented with 100, 500, or 1000 pg/ml melatonin for 7 days. PI3K inhibition was performed through pretreatment of ovarian fragments with LY294002. Thereafter, immunohistochemistry was performed to evaluate the expression of cleaved caspase-3, Akt, phosphorylated-Akt, and phosphorylated-FOXO3a (p-FOXO3a). The immunohistochemical localization of the MT 1 receptor protein was documented in sheep preantral and antral follicles. After in vitro culture, 100 pg/ml melatonin showed higher follicular survival and activation than α-MEM + and other melatonin concentrations.After PI3K inhibition, there was an increase in cleaved caspase-3-positive follicles, and a decrease in the primordial follicle activation, Akt phosphorylation, and nuclear exclusion of p-FOXO3a. In conclusion, MT 1 receptor protein is present in the sheep ovary.Furthermore, 100 pg/ml melatonin maintains survival and stimulates activation of primordial follicles through the PI3K/Akt/FOXO3a signaling pathway after in vitro culture of sheep ovarian tissue. K E Y W O R D S hormone receptor, immunohistochemistry, in vitro culture, ovarian cortex, preantral follicle 1 | INTRODUCTION In vitro activation of primordial follicles cultured within the ovary itself is an essential tool to study the early follicle development and optimize the use of the female germ cell pool (Telfer & Zelinski, 2013; J. J. Wang et al., 2017). Studies on in vitro activation of primordial follicles, and subsequent growth and maturation have gained a lot of attention as a potential source of mature eggs for in vitro fertilization and embryo transfer, followed by the delivery of healthy born

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Melatonin promotes proliferation of neural stem cells from adult mouse spinal cord via the PI3K/AKT signaling pathway

Cited by 17 publications

References 35 publications

Melatonin and the Programming of Stem Cells

Melatonin and the Programming of Stem Cells

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

Immunolocalization of melatonin receptor type 1 in the sheep ovary and involvement of the PI3K/Akt/FOXO3a signaling pathway in the effects of melatonin on survival and in vitro activation of primordial follicles

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