NT-3 attenuates the growth of human neuron cells through the ERK pathway

Li, Ruifeng; Wu, Yimin; Jiang, Dianming

doi:10.1007/s10616-014-9813-1

Cited by 8 publications

(6 citation statements)

References 16 publications

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“…ERK and Akt played an important role in cell proliferation, apoptosis, migration and staying cell morphology. ERK and Akt were activated through phosphorylating tyr202/204 and ser473 residues, respectively, and exerted their functions [ 20 , 21 ]. We evaluated the expression levels of total ERK and p-ERK by Western blot after treated with AT-II for 48 h. The activation level of ERK was downregulated significantly by AT-II in a dose-dependent manner.…”

Section: Resultsmentioning

confidence: 99%

Atractylenolide II Inhibits Proliferation, Motility and Induces Apoptosis in Human Gastric Carcinoma Cell Lines HGC-27 and AGS

Shen

Hongdan

2017

Molecules

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Atractylenolide II (AT-II) exhibits several biological and pharmacological functions, especially anti-cancer activity as the major sesquiterpene lactones isolated from Atractylodes macrocephala (also named Baizhu in Chinese). However, the effects and mechanisms of AT-II on human gastric cancer remain unclear. Cell Counting Kit-8 (CCK-8) assay, morphological changes, flow cytometry, wound healing assay and Western blot analysis were used to investigate the effects of AT-II on cell proliferation, apoptosis and motility of human gastric carcinoma cell lines HGC-27 and AGS. Our results indicated that AT-II could significantly inhibit cell proliferation, motility and induce apoptosis in a dose and time-dependent manner. Western blot analysis showed that the expression level of Bax was upregulated and the expression levels of B-cell lymphoma-2 (Bcl-2), phosphorylated-protein kinase B (p-Akt) and phosphorylated-ERK (p-ERK) were downregulated compared to control group. In conclusion, the findings suggested that AT-II exerted significant anti-tumor effects on gastric carcinoma cells by modulating Akt/ERK signaling pathway, which might shed light on therapy of gastric carcinoma.

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Section: Resultsmentioning

confidence: 99%

Atractylenolide II Inhibits Proliferation, Motility and Induces Apoptosis in Human Gastric Carcinoma Cell Lines HGC-27 and AGS

Shen

Hongdan

2017

Molecules

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“…Several studies have shown that NT-3 binds to TrkC, triggers the receptor and signals cascades (Ivanov et al 2013;Han et al 2016;Li et al 2016). To identify the signaling pathway through which NT-3 on 661W cells, cells were treated with exogenous NT-3 (20 nM) for 24 h and the phosphorylation state of the mitogenactivated protein kinase (MAPK) signaling pathway was examined, including ERK1/2, p38 and JNK.…”

Section: Nt-3 Inhibited the Apoptosis Of 661w Cells Via Erk1/2 Pathwaymentioning

confidence: 99%

Müller cells derived neurotrophin-3 inhibits hypoxia-induced photoreceptor apoptosis via the TrkC/ERK pathway

Zhu

Wang

et al. 2019

Cytotechnology

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, a neurotrophic factor that mainly binds to the tyrosine kinase C (trkC) receptor, has been shown to play a crucial role in proliferation, differentiation, and survival. However, the role of NT-3 in the hypoxia-induced retinopathy has not been investigated extensively.Here, we created a model of hypoxia (1% O 2 ) in vitro and found that hypoxia promoted the apoptosis of mouse cone photoreceptor-derived 661W cells, increased the expression of TrkC and cleaved caspase-3. In contrast, the hypoxia-mediated 661W cell apoptosis was markedly alleviated by co-culturing with primary mouse Mu ¨ller cells. Further mechanism studies revealed that hypoxia increased the synthesis and secretion of NT-3 by Mu ¨ller cells, and exogenous NT-3 stimulation increased the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 by binding to TrkC in 661W cells. Besides, both siRNA knockdown of TrkC expression and incubation with an ERK-specific inhibitor PD98059 triggered apoptosis in hypoxic 661W cells. Altogether, these data suggest that NT-3 originating from Mu ¨ller cells protects photoreceptors from hypoxia-induced apoptosis through a TrkC/ERK-dependent pathway. Our findings may facilitate future studies on the therapeutic implications of NT-3 in the treatment of hypoxiarelevant retinal diseases.

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“…Impaired ERK Activation in Pyramidal mPFC-IL Neurons of TgNTRK3 Mice ERK activation, which can be triggered by the NT3/TrkC intracellular signaling cascade (Li et al, 2014;Reichardt, 2006), is necessary for successful fear extinction in rodents (Fischer et al, 2007;Tronson et al, 2009). We therefore reasoned that altered NT3/TrkC function might disturb fear extinction memory in TgNTRK3 mice due to impaired ERK signaling.…”

Section: Acquisition Of Contextual Fear Conditioning and Extinction Rmentioning

confidence: 99%

“…First, we observed that TgNTRK3 did not show the extinction-related increase in NT3 levels in the mPFC that we observed in WT animals. Binding of NT3 to its highaffinity TrkC receptor results in intracellular activation of ERK signaling (Li et al, 2014;Reichardt, 2006). Therefore, the NT3 deficit observed in TgNTRK3 animals is likely to result in a deficit in the activation of the NT3/TrkC downstream pathway ERK.…”

Section: Impaired Fear Extinction Rescue Via Nt3/trkc-erk Pathway D Dmentioning

confidence: 99%

Infralimbic Neurotrophin-3 Infusion Rescues Fear Extinction Impairment in a Mouse Model of Pathological Fear

D’Amico

Gener

Lagrán

et al. 2016

Neuropsychopharmacol

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The inability to properly extinguish fear memories constitutes the foundation of several anxiety disorders, including panic disorder. Recent findings show that boosting prefrontal cortex synaptic plasticity potentiates fear extinction, suggesting that therapies that augment synaptic plasticity could prove useful in rescue of fear extinction impairments in this group of disorders. Previously, we reported that mice with selective deregulation of neurotrophic tyrosine kinase receptor, type 3 expression (TgNTRK3) exhibit increased fear memories accompanied by impaired extinction, congruent with an altered activation pattern of the amygdala-hippocampus-medial prefrontal cortex fear circuit. Here we explore the specific role of neurotrophin 3 and its cognate receptor in the medial prefrontal cortex, and its involvement in fear extinction in a pathological context. In this study we combined molecular, behavioral, in vivo pharmacology and ex vivo electrophysiological recordings in TgNTRK3 animals during contextual fear extinction processes. We show that neurotrophin 3 protein levels are increased upon contextual fear extinction in wild-type animals but not in TgNTRK3 mice, which present deficits in infralimbic long-term potentiation. Importantly, infusion of neurotrophin 3 to the medial prefrontal cortex of TgNTRK3 mice rescues contextual fear extinction and ex vivo local application improves medial prefrontal cortex synaptic plasticity. This effect is blocked by inhibition of extracellular signal-regulated kinase phosphorylation through peripheral administration of SL327, suggesting that rescue occurs via this pathway. Our results suggest that stimulating neurotrophin 3-dependent medial prefrontal cortex plasticity could restore contextual fear extinction deficit in pathological fear and could constitute an effective treatment for fear-related disorders.

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NT-3 attenuates the growth of human neuron cells through the ERK pathway

Cited by 8 publications

References 16 publications

Atractylenolide II Inhibits Proliferation, Motility and Induces Apoptosis in Human Gastric Carcinoma Cell Lines HGC-27 and AGS

Atractylenolide II Inhibits Proliferation, Motility and Induces Apoptosis in Human Gastric Carcinoma Cell Lines HGC-27 and AGS

Müller cells derived neurotrophin-3 inhibits hypoxia-induced photoreceptor apoptosis via the TrkC/ERK pathway

Infralimbic Neurotrophin-3 Infusion Rescues Fear Extinction Impairment in a Mouse Model of Pathological Fear

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