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Positive feedback regulation of Akt‐FMRP pathway protects neurons from cell death
Jeon, Se Jin,Han, Seol‐,Heui,Yang, Sung‐,Il,Choi, Ji woong,Kwon, Kyoung Ja,Park, Seung Hwa,Kim, Hahn Young,Cheong, Jae Hoon,Ryu, Jong Hoon,Ko, Kwang Ho,Wells, David G,Shin, Chan Young Blackwell Publishing Ltd 2012 Journal of Neurochemistry Vol.123 No.2
<P><I>J. Neurochem.</I> (2012) <B>123</B>, 226–238.</P><P><B>Abstract</B></P><P>Fragile X syndrome (FXS), the most common single genetic cause of mental retardation and autistic spectrum disease, occurs when <I>FMR1</I> gene is mutated. <I>FMR1</I> encodes fragile X mental retardation protein (FMRP) which regulates translation of mRNAs playing important roles in the development of neurons as well as formation and maintenance of synapses. To examine whether FMRP regulates cell viability, we induced apoptosis in rat primary cortical neurons with glutamate <I>in vitro</I> and with middle cerebral artery occlusion (MCAO) in striatal neurons <I>in vivo</I>. Both conditions elicited a rapid, but transient FMRP expression in neurons. This up‐regulated FMRP expression was abolished by pre‐treatment with PI3K and Protein Kinase B (Akt) inhibitors: LY294002, Akt inhibitor IV, and VIII. Reduced FMRP expression <I>in vitro</I> or <I>in vivo</I> using small hairpin <I>Fmr1</I> virus exacerbated cell death by glutamate or MCAO, presumably <I>via</I> hypophosphorylation of Akt and reduced expression of B‐cell lymphoma‐extra large (Bcl‐xL). However, over‐expression of FMRP using enhanced green fluorescent protein (eGFP)‐FMRP constructs alleviated cell death, increased Akt activity, and enhanced Bcl‐xL production. The pro‐survival role of Akt‐dependent up‐regulation of FMRP in glutamate‐stimulated cultured neuron as well as in ischemic brain may have a clinical importance in FXS as well as in neurodegenerative disorders and traumatic brain injury.</P>
( Se Jin Jeon ),( Hae Rang Bak ),( Jung Eun Seo ),( So Min Han ),( Sung Hoon Lee ),( Seol Heui Han ),( Kyoung Ja Kwon ),( Jong Hoon Ryu ),( Jae Hoon Cheong ),( Kwang Ho Ko ),( Sung Il Yang ),( Ji Woon 한국응용약물학회 2012 Biomolecules & Therapeutics(구 응용약물학회지) Vol.20 No.1
Oroxylin A is a flavone isolated from a medicinal herb reported to be effective in reducing the inflammatory and oxidative stresses. It also modulates the production of brain derived neurotrophic factor (BDNF) in cortical neurons by the transactivation of cAMP response element-binding protein (CREB). As a neurotrophin, BDNF plays roles in neuronal development, differentiation, synaptogenesis, and neural protection from the harmful stimuli. Adenosine A2A receptor colocalized with BDNF in brain and the functional interaction between A2A receptor stimulation and BDNF action has been suggested. In this study, we investigated the possibility that oroxylin A modulates BDNF production in cortical neuron through the regulation of A2A receptor system. As expected, CGS21680 (A2A receptor agonist) induced BDNF expression and release, however, an antagonist, ZM241385, prevented oroxylin A-induced increase in BDNF production. Oroxylin A activated the PI3K-Akt-GSK-3β signaling pathway, which is inhibited by ZM241385 and the blockade of the signaling pathway abolished the increase in BDNF production. The physiological roles of oroxylin A-induced BDNF production were demonstrated by the increased neurite extension as well as synapse formation from neurons. Overall, oroxylin A might regulate BDNF production in cortical neuron through A2A receptor stimulation, which promotes cellular survival, synapse formation and neurite extension.
Jeon, Se Jin,Park, Ho Jae,Gao, Qingtao,Lee, Hyung Eun,Park, Se Jin,Hong, Eunyoung,Jang, Dae Sik,Shin, Chan Young,Cheong, Jae Hoon,Ryu, Jong Hoon Elsevier 2015 Behavioural brain research Vol.291 No.-
<P><B>Abstract</B></P> <P>Sleep loss, insomnia, is considered a sign of imbalance of physiological rhythm, which can be used as pre-clinic diagnosis of various neuropsychiatric disorders. The aim of the present study is to understand the pharmacological actions of α- or β-amyrin, natural triterpene compound, on the sleep in mice. To analyze the sleeping behavior, we used the well-known pentobarbital-induced sleeping model after single administration of either α- or β-amyrin. The sleeping onset time was remarkably decreased and duration was prolonged by β-amyrin (1, 3, or 10mg/kg) but not by α-amyrin (1, 3, or 10mg/kg). These effects were significantly blocked by GABA<SUB>A</SUB> receptor antagonist, bicuculline. Moreover, β-amyrin increased brain GABA level compared to the vehicle administration. Overall, the present study suggests that β-amyrin would enhance the total sleeping behavior in pentobarbital-induced sleeping model via the activation of GABAergic neurotransmitter system through GABA content in the brain.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Pentobarbital-induced sleeping behavior was prolonged by β-amyrin. </LI> <LI> Increased sleeping behavior was blocked by GABA<SUB>A</SUB> receptor antagonist. </LI> <LI> Brain GABA level was increased by β-amyrin administration. </LI> </UL> </P>
Jeon, Se-Hoon,Kim, Ui-Seong,Jeon, Won-Jin,Shin, Chee-Burm,Hong, Su-Rin,Choi, In-Hee,Lee, Su-Seung,Yi, Jong-Heop The Polymer Society of Korea 2009 Macromolecular Research Vol.17 No.3
Recently, the multi-screening of target materials has been made possible by the development of the surface plasmon resonance (SPR) imaging method. To adapt this method to biochemical analysis, the multi-patterning technology of protein microarrays is required. Among the different methods of fabricating protein microarrays, the microfluidic platform was selected due to its various advantages over other techniques. Microfluidic devices were designed and fabricated with polydimethylsiloxane (PDMS) by the replica molding method. These devices were designed to operate using only capillary force, without the need for additional flow control equipment. With these devices, multiple protein-patterned sensor surfaces were made, to support the two-dimensional detection of various protein-protein interactions with SPR. The fabrication technique of protein microarrays can be applied not only to SPR imaging, but also to other biochemical analyses.
Jeon, Se Jin,Lee, Hong Ju,Lee, Hyung Eun,Park, Se Jin,Gwon, Yubeen,Kim, Haneul,Zhang, Jiabao,Shin, Chan Young,Kim, Dong Hyun,Ryu, Jong Hoon Elsevier 2017 NEUROPHARMACOLOGY - Vol.113 No.1
<P><B>Abstract</B></P> <P>Oleanolic acid is a naturally occurring triterpenoid and is widely present in food and medicinal plants. To examine the effect of oleanolic acid on memory deficits, we employed a cholinergic blockade-induced cognitive deficit mouse model. A single administration of oleanolic acid significantly increased the latency on the passive avoidance task and affected the alternation behavior on the Y-maze task and the exploration time on the novel object recognition task, indicating that oleanolic acid reverses the cognitive impairment induced by scopolamine. In accordance with previous reports, oleanolic acid enhanced extracellular-signal-regulated kinase 1/2 <B>(</B>ERK1/2) and cAMP response element-binding protein (CREB) phosphorylation and brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Interestingly, ameliorating effect of oleanolic acid on scopolamine-induced memory impairment was abolished by N2-(2-{[(2-oxoazepan-3-yl)amino]carbonyl}phenyl)benzo[<I>b</I>]thiophene-2-carboxamide (ANA-12), a potent and specific inhibitor of tropomyosin receptor kinase B (TrkB), in the passive avoidance task. Similarly, oleanolic acid significantly evoked long-term potentiation in a dose-dependent manner, which was diminished by ANA-12 treatment as shown in the electrophysiology study. Together, these results imply that oleanolic acid ameliorates scopolamine-induced memory impairment by modulating the BDNF-ERK1/2-CREB pathway through TrkB activation in mice, suggesting that oleanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Oleanolic acid activated the ERK1/2-CREB-BDNF pathway in the hippocampus via TrkB activation. </LI> <LI> Scopolamine-induced memory dysfunction was ameliorated by oleanolic acid treatment. </LI> <LI> Oleanolic acid evoked the long-term potentiation in a dose-dependent manner. </LI> <LI> Oleanolic acid would be a potential therapeutic agent for the cognitive problem. </LI> </UL> </P>
이세훈(Se-Hoon Lee),전상표(Sang-Pyo Jeon),신영진(Young-Jin Shin),박전진(Jeon-Jin Park) 한국컴퓨터정보학회 2010 한국컴퓨터정보학회 학술발표논문집 Vol.18 No.2
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