Brain-derived Neurotrophic Factor Promotes Growth of Neurons and Neural Stem Cells Possibly by Triggering the Phosphoinositide 3-Kinase/ AKT/Glycogen Synthase Kinase-3β/β-catenin Pathway

Li, Xing-Tong; Liang, Zhen; Wang, Tongtong; Yang, Jinwei; Ma, Wei; Deng, Shi-Kang; Wang, Xianbin; Dai, Yunfei; Guo, Jun; Li, Liyan

doi:10.2174/1871527316666170518170422

Cited by 36 publications

(29 citation statements)

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“…At the same time, the receptor of BDNF, tropomyosin receptor kinase B (TrkB), was expressed in NSPCs. It has been reported that BDNF/Akt signaling was related to NSPC growth and differentiation in vitro, and BDNF secretion as well as the phosphorylation of Akt could be induced by different frequency magnetic stimulation, followed by an influence on neuronal cell proliferation (Sabelström et al, 2014;Hossain et al, 2017;Li et al, 2017). Our results confirmed that the phosphorylation of Akt at Thr308 and Ser473 sites was increased upon magnetic stimulation.…”

Section: Discussionsupporting

confidence: 86%

rTMS Regulates the Balance Between Proliferation and Apoptosis of Spinal Cord Derived Neural Stem/Progenitor Cells

Zhao

Qin

Sun

et al. 2020

Front. Cell. Neurosci.

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Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive technique that uses electromagnetic fields to stimulate the brain. rTMS can restore an impaired central nervous system and promote proliferation of neural stem/progenitor cells (NSPCs), but optimal stimulus parameters and mechanisms underlying these effects remain elusive. The purpose of this study is to investigate the effect of different rTMS stimulus parameters on proliferation and apoptosis of spinal cord-derived NSPCs, the expression of brain-derived neurotrophic factor (BDNF) after rTMS, and the potentially underlying pathways. NSPCs were isolated from mice spinal cord and stimulated by different frequencies (1/10/20 Hz), intensities (0.87/1.24/1.58 T), and number of pulses (400/800/1,500/3,000) once a day for five consecutive days. NSPC proliferation was analyzed by measuring the neurosphere diameter and Brdu staining, apoptosis was detected by cell death enzyme-linked immunosorbent assay (ELISA) and flow cytometry, and NSPC viability was assessed by cell counting kit-8 assay. We found that specific parameters of frequency (1/10/20 Hz), intensity (1.24/1.58 T), and number of pulses (800/1,500/3,000) promote proliferation and apoptosis (p < 0.05 for all), but 20 Hz, 1.58 T, and 1,500 pulses achieved the optimal response for the NSPC viability. In addition, rTMS significantly promoted the expression of BDNF at the mRNA and protein level, while also increasing Akt phosphorylation (Thr308 and Ser473; p < 0.05). Overall, we identified the most appropriate rTMS parameters for further studies on NSPCs in vitro and in vivo. Furthermore, the effect of magnetic stimulation on NSPC proliferation might be correlated to BDNF/Akt signaling pathway.

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Section: Discussionsupporting

confidence: 86%

rTMS Regulates the Balance Between Proliferation and Apoptosis of Spinal Cord Derived Neural Stem/Progenitor Cells

Zhao

Qin

Sun

et al. 2020

Front. Cell. Neurosci.

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“…Bdnf ) expression (Zhang, Zhang, Deng, et al, ; Zhang, Shi, et al, ; Zhang, Zhang, Yang, et al, ). Also, in human NSCs, Yang et al () showed the ability of BDNF to promote their growth via GSK‐3β‐mediated crosstalk with the WβC‐ signalling pathway, and Li et al () involved the contribution of the PI3K/Akt/GSK‐3β/β‐catenin pathway in BDNF‐induced neuron and NSC growth. Ambrosone et al () documented the ability of optogenetic stimulation to promote cell proliferation and the migration of SVZ neuroblasts into the peri‐infarct cortex, asssociated with increased neuronal differentiation and improvement of long‐term functional recovery after stroke.…”

Section: Therapeutic Modulation Of Wnt/β‐catenin Signallingmentioning

confidence: 99%

“…Physical activity and environmental enrichment regulate the generation of neural precursors in the adult mouse substantia nigra; WβC-AC involvement to be elucidated Klaissle et al (2012) Endurance exercise promotes neuroprotection against MPTP injury via enhanced neurogenesis, antioxidant capacity and autophagy; WβC-AC involvement to be elucidated Jang, kwon, Song, Cosio-Lima and Lee (2018a), Jang et al (2018b) Neural activation Neural activity-induced WβC-AC up-regulates expression of BDNF. Zhang, Zhang, Deng, et al, 2018a Neurotrophic factors BDNF promotes growth of neurons and NSCs, possibly through activation of the PI3K/GSK-3β/β-catenin pathway Li et al (2017) BDNF promotes human neural stem cell growth via GSK-3β-mediated crosstalk with the WβC pathway Yang et al (2016) Optical depolarization…”

Section: Optogeneticsmentioning

confidence: 99%

Parkinson's disease, aging and adult neurogenesis: Wnt/β‐catenin signalling as the key to unlock the mystery of endogenous brain repair

et al. 2020

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A common hallmark of age‐dependent neurodegenerative diseases is an impairment of adult neurogenesis. Wingless‐type mouse mammary tumor virus integration site (Wnt)/β‐catenin (WβC) signalling is a vital pathway for dopaminergic (DAergic) neurogenesis and an essential signalling system during embryonic development and aging, the most critical risk factor for Parkinson's disease (PD). To date, there is no known cause or cure for PD. Here we focus on the potential to reawaken the impaired neurogenic niches to rejuvenate and repair the aged PD brain. Specifically, we highlight WβC‐signalling in the plasticity of the subventricular zone (SVZ), the largest germinal region in the mature brain innervated by nigrostriatal DAergic terminals, and the mesencephalic aqueduct‐periventricular region (Aq‐PVR) Wnt‐sensitive niche, which is in proximity to the SNpc and harbors neural stem progenitor cells (NSCs) with DAergic potential. The hallmark of the WβC pathway is the cytosolic accumulation of β‐catenin, which enters the nucleus and associates with T cell factor/lymphoid enhancer binding factor (TCF/LEF) transcription factors, leading to the transcription of Wnt target genes. Here, we underscore the dynamic interplay between DAergic innervation and astroglial‐derived factors regulating WβC‐dependent transcription of key genes orchestrating NSC proliferation, survival, migration and differentiation. Aging, inflammation and oxidative stress synergize with neurotoxin exposure in “turning off” the WβC neurogenic switch via down‐regulation of the nuclear factor erythroid‐2‐related factor 2/Wnt‐regulated signalosome, a key player in the maintenance of antioxidant self‐defense mechanisms and NSC homeostasis. Harnessing WβC‐signalling in the aged PD brain can thus restore neurogenesis, rejuvenate the microenvironment, and promote neurorescue and regeneration.

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“…Sevoflurane was also reported to decrease the level of BDNF and induced cognitive impairment in 18 month-old rats [45]. BDNF is critical involved in the differentiation of NSCs from iPSCs [47] and could promote neurons and NSCs growth [48]. We further found that miR-466l -3p directly targets BDNF, leading to the inhibition of the neural differentiation.…”

Section: Discussionmentioning

confidence: 72%

“…Next, we addressed which downstream target gene could be regulated by miR-466l-3p. Brain derived neurotrophic factor (BDNF) is critical involved in the differentiation of iPSCs to NSCs [47] and also promotes growth of neurons and NSCs [48]. Sevoflurane also resulted in significant inhibition BDNF expression and cognitive impairment [45].…”

Section: Bdnf Is Directly Targeted By Mir-466l-3p To Mediate Neural Dmentioning

confidence: 99%

Sevoflurane regulating LncRNA Rik-203 contributes to neural differentiation via microRNA-466l-3p /BDNF pathway

Zhang

Liu

Xue

et al. 2019

Preprint

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Background: The anesthetics inhibit neural differentiation, induced neuron loss and cognitive impairment in young animals. However, the underlying mechanisms of anesthesia on neural differentiation and are unknown. Methods: Embryonic stem cells (ESCs) and mice received sevoflurane anesthesia. RNA sequencing; gene expression of mRNAs, LncRNAs and miRNAs; over-expression and RNA interference of genes; flow cytometry; real-time quantity PCR and Western blot were used in the studies. RNA pull-down assay and PCR were employed to detect any miRNA that attached to Rik-203. The binding of miRNA with mRNA of BDNF was presented by the luciferase assay. Results: Here we found that LncRNA Rik-203 was higher expressed in mice brain than other tissues and increased during neural differentiation. Sevoflurane decreased the level of Rik-203 in mice brain. Knockdown of Rik-203 repressed the neural differentiation derived from mouse embryonic stem cell with the downregulation of the neural progenitor cells markers Sox1 and Nestin. RNA pull-down showed that miR-466l-3p was highly bound to Rik-203 and mediated the function of Rik-203. Inhibition of miR-466l-3p restored the neural differentiation repressed by Rik-203 knockdown. BDNF was directly targeted by miR-466l-3p and also downregulated by sevoflurane. Overexpression of BDNF restored the neural differentiation repressed by miR-466l-3p and Rik-203 knockdown. Conclusion: Our study suggested that sevoflurane related LncRNARik-203 facilitates neural differentiation by inhibiting miR-466l-3p’s ability to reduce BDNF levels. Keywords: Anesthesia; sevoflurane; Rik-203; miR-466l-3p; BDNF; neural differentiation.

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Brain-derived Neurotrophic Factor Promotes Growth of Neurons and Neural Stem Cells Possibly by Triggering the Phosphoinositide 3-Kinase/ AKT/Glycogen Synthase Kinase-3β/β-catenin Pathway

Abstract: Our findings suggested that BDNF contributed to neuronal growth and proliferation and differentiation of NSCs in vitro by stimulating PI3K/AKT/GSK3β/β-catenin pathways.

Cited by 36 publications

References 0 publications

rTMS Regulates the Balance Between Proliferation and Apoptosis of Spinal Cord Derived Neural Stem/Progenitor Cells

rTMS Regulates the Balance Between Proliferation and Apoptosis of Spinal Cord Derived Neural Stem/Progenitor Cells

Parkinson's disease, aging and adult neurogenesis: Wnt/β‐catenin signalling as the key to unlock the mystery of endogenous brain repair

Sevoflurane regulating LncRNA Rik-203 contributes to neural differentiation via microRNA-466l-3p /BDNF pathway

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