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1. Update on Alzheimer's neurodegeneration induced by amyloid precursor protein | |||
ZHAO Dan,ZHAO Jie,LI Shao | |||
Basic Medicine 27 May 2016 | |||
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Abstract:The loss of synapses between neurons as well as progressive neuronal degeneration and apoptosis is the basis of pathological Alzheimer's disease (AD), which directly induces progressive memorial and cognitive impairment of AD patients. Beta amyloid precursor protein (β-APP,APP) is commonly associated with senile plaques formation which is best known for the pathogenesis of AD. More and more studies have shown that the structure and the hydrolysic way of APP play very important roles in neuronal degeneration and apoptosis of AD by many ways. In this paper, we will overview the update progress for the pathophysiological mechanism of neuronal degeneration and apoptosis induced by APP, from the perspective of APP structure and its hydrolysis. | |||
TO cite this article:ZHAO Dan,ZHAO Jie,LI Shao. Update on Alzheimer's neurodegeneration induced by amyloid precursor protein[OL].[27 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693086 |
2. Potassium Channels Depression is involved in the Apolipoprotein E4 enhanced Calcium Influx via N-Methyl-D-Aspartate receptor | |||
Qin Ying,Yang Lifan,Weng Yuteng,Luo Xiaoli | |||
Basic Medicine 29 January 2014 | |||
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Abstract:Among many suggested mechanisms of the association between the ε4 allele of apoplipoprotein E gene (APOE) and Alzheimer's disease (AD), the present study focused on the link of apoE4 to Ca2+ homeostasis. On the acutely isolated hippocampal neurons, our observation showed that: 1) apoE4 increased the [Ca2+]i greatly and immediately. It was in a dose- and time- dependent manner, and irreversible; 2) removing Ca2+ from external solution abolished apoE4's effect on [Ca2+]i; 3) nicardipine showed little effect on apoE4-elicited [Ca2+]i increasing, while MK-801 almost blocked the apoE4-induced Ca2+ influx; and 4) pretreatment with K+ channel opener significantly reduced the apoE4-induced [Ca2+]i increasing. The results suggest that apoE4 increased [Ca2+]i by way of NMDA receptor channels but not L-type Ca2+ channels; and the depression of K+ channel activities was involved in this effects of apoE4. | |||
TO cite this article:Qin Ying,Yang Lifan,Weng Yuteng, et al. Potassium Channels Depression is involved in the Apolipoprotein E4 enhanced Calcium Influx via N-Methyl-D-Aspartate receptor[OL].[29 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4584364 |
3. Apolipoprotein E4 Suppresses potassium currents in Hippocampal Neurons | |||
Qin Ying,Xie Dongping,Weng Yuteng,Luo Xiaoli,Yang Lifan | |||
Basic Medicine 13 January 2014 | |||
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Abstract:apolipoprotein E epsilon 4 allele (APOE4) is one of the major risk factors for Alzheimer's disease,but the underlying mechanism remains unclear. Our data show that: 1) application of apoE4 in extracellular solution suppresses the delayed rectifier potassium current (synonym: IK) by 18.9± 2.8 % and 18.1 ± 3.6 % (n=10, P<0.01), at +30 mV and +60 mV of membrane potential. The effect is reversible and shows no voltage-dependency; 2) extracellular application of apoE4 does not show any obvious effect on A-type fast transient potassium current (synonym: IA); 3) application of apoE4 in the intracellular solution suppresses both IA and IK. In case of IK, the reduction rate is 56.2 ± 7.6 % and 58.7 ± 7.4 % (n=10, P<0.01) at +30 mV and +60 mV of membrane potential, respectively; in case of IA, the reductive rate is 58.6 ± 9.7 % and 65.3 ± 8.6 % (n=10, P<0.01) at +30 mV and +60 mV, respectively; 4) the effects of intracellular apoE4 on both IA and IK show obvious voltage-dependent; and 5) in the contrast, application of apoA and apoE3 exhibits no effects on IK or IA. The results indicate that apoE4 molecules could suppress the potassium currents from neurons on both the inner and outer side of neuronal membrane, which support the propulsions that apoE4 expressed by neurons might be responsible for neuronal damages related to the pathogenesis of Alzheimer's disease. | |||
TO cite this article:Qin Ying,Xie Dongping,Weng Yuteng, et al. Apolipoprotein E4 Suppresses potassium currents in Hippocampal Neurons[OL].[13 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581917 |
4. Iron status and lipopolysaccharide regulate Ndfip1 by activation of nuclear factor-kappa B | |||
XU Huamin,CHANG Qing,JIA Wenting,JIANG Hong,SUN Peng,XIE Junxia | |||
Basic Medicine 30 August 2013 | |||
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Abstract:Nedd4 family interacting protein 1 (Ndfip1) is an adaptor protein for the Nedd4 family of ubiquitin ligases that target proteins for degradation. Recent studies confirmed the role of Ndfip1 as a regulator of iron metabolism and pointed out that Ndfip1 was involved in iron homeostasis by regulating the degradation of iron importer divalent metal transporter 1 (DMT1). However, little is known about how Ndfip1 is regulated. The aim of this article was to investigate the regulation of Ndfip1 levels and the possible mechanisms. In this study, we investigated the effect of various stimuli, including iron status and lipopolysaccharide (LPS) on Ndfip1 expression in MES23.5 dopaminergic cell lines. Results showed that Ndfip1 expression in these cells was enhanced by ferrous iron overload, but not ferric iron overload, and decreased after iron deprivation by desferoxamine (DFO). In addition, LPS could significantly increase the expression of Ndfip1. Furthermore, we demonstrated that the regulation of Ndfip1 expression by these various stimuli was achieving by activation of nuclear factor-kappa B. We speculate that iron status and LPS may contribute to the changes of Ndfip1 expression by activation of nuclear factor-kappa B. | |||
TO cite this article:XU Huamin,CHANG Qing,JIA Wenting, et al. Iron status and lipopolysaccharide regulate Ndfip1 by activation of nuclear factor-kappa B[OL].[30 August 2013] http://en.paper.edu.cn/en_releasepaper/content/4557706 |
5. Case-control study of FGF20 polymorphism in sporadic Parkinson's disease in Northern Han Chinese | |||
XU Xiaofeng,XU Huamin,XIE Anmu,JIANG Hong,XIE Junxia | |||
Basic Medicine 07 March 2013 | |||
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Abstract:Fibroblast growth factor 20 (FGF20) is a neurotrophic factor that exerts neurotrophic properties in the brain and could significantly enhance the survival of rat midbrain dopaminergic neurons. The genetic association of the FGF20 gene with Parkinson's disease (PD) remains controversial. Herein we used polymerase chain reaction-restriction length polymorphism assay to assess the association of two single nucleotide polymorphisms (SNPs) rs12720208 and rs1721100 within FGF20 gene in 178 PD patients and 190 healthy controls in Northern Han Chinese. Results showed no significant differences in the rs1721100 or rs12720208 of FGF20 gene between PD cases and the controls. This indicates FGF20 gene might not play a major role in the genetic predisposition to PD in this population. | |||
TO cite this article:XU Xiaofeng,XU Huamin,XIE Anmu, et al. Case-control study of FGF20 polymorphism in sporadic Parkinson's disease in Northern Han Chinese[OL].[ 7 March 2013] http://en.paper.edu.cn/en_releasepaper/content/4527523 |
6. 6-Hydroxydopamine Promotes Iron Traffic in Primary Cultured Astrocytes | |||
ZHANG Haoyun,SONG Ning,XU Huamin,SHI Limin,JIANG Hong,XIE Junxia | |||
Basic Medicine 06 March 2013 | |||
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Abstract:It is well known that disrupted brain iron homeostasis was involved in Parkinson's disease (PD). Astrocytes, the major glial cell type in the central nervous system, are largely responsible for iron distribution in the brain. However, how iron metabolism changes of astrocytes in PD are not fully elucidated. In the present study, we first observed that both iron influx and efflux were enhanced with 10 μM 6-OHDA treatment for 24 hrs in primary cultured astrocytes. In accordance with this iron traffic modulations, iron importer divalent metal transporter 1 with iron responsive element (DMT1+IRE) and exporter ferroportin 1 (FPN1) were up-regulated in these cells. Iron regulatory protein 1 (IRP1) showed a dynamic regulation with 6-OHDA treatment, as indicated by a moderate up-regulation at 12 hrs, however, down-regulation at 24 hrs. These results suggest that 6-OHDA might promote iron transport rate in astocytes by regulating iron transporters and IRP1 expression. | |||
TO cite this article:ZHANG Haoyun,SONG Ning,XU Huamin, et al. 6-Hydroxydopamine Promotes Iron Traffic in Primary Cultured Astrocytes[OL].[ 6 March 2013] http://en.paper.edu.cn/en_releasepaper/content/4527136 |
7. Inhibition of gastric motility by endogenous H2S via enteric nervous system | |||
YE Yanfang,LU Wen,ZHU Jianchun,DU Yahui,LIU Kejing,QIN Junfang,FENG Mei,LUO Yan,LIU Chuanyong | |||
Basic Medicine 17 January 2013 | |||
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Abstract:Hydrogen Sulfide (H2S) might be a gastrotransmitter in enteric nervous system and might be involved in the regulation of gastrointestinal motility and secretion. This study was conducted to investigate the effect of endogenous H2S on gastric motility. Methods. In in vivo experiments, the intragastric pressure of rats were monitored, and in in vitro experiments, the spontaneous contraction of muscle strips of gastric body was recorded. The location of cystathionine-beta-synthetase (CSE) and cystathionine-gama-lyase (CBS) in stomach was studied by immnohistochemistry staining and Western blot. Key Results: Systemic L-cysteine (100 μmol /kg,i.p.) significantly decreased intragastric pressure. In vitro, L-cysteine (10-4 M- 5×10-3 M) and S-adenosyl-l-methionine (SAM) (5 × 10-4 M - 5 × 10-3 M) significantly decreased the tension of the muscle strips from gastric body. This effect of L-cysteine on muscle strip was not influenced by pretreatment of L-NAME and glibenclamide but was reversed by TTX. In in vitro experiments, administration of PAG (10-6 M-10-3 M), the specific inhibitor of CSE, or AOAA (10-6 M), the specific inhibitor of CBS, significantly increased the mean tension of gastric muscle strips. Both PAG and AOAA significantly reversed the inhibitory effect of L-cysteine on gastric motility in vitro. Both CBS and CSE were located in the myenteric plexus of stomach. Conclusions & Inferences : We concluded that endogenous H2S inhibited gastric motility via ENS. H2S might be a physiologic relaxant of gastric smooth muscle and exert tonic inhibition on gastric motility. | |||
TO cite this article:YE Yanfang,LU Wen,ZHU Jianchun, et al. Inhibition of gastric motility by endogenous H2S via enteric nervous system[OL].[17 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4515344 |
8. Differential effects of anandamide and WIN 55,212-2 on hippocampal CA1 long-term potentiation in vivo | |||
Wang Wei,Liu Changjin | |||
Basic Medicine 27 January 2011 | |||
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Abstract:Cannabinoids are believed to alter cognition and prevent long-term potentiation (LTP) via cannabinoid receptor (CB1) activation, but the effects of endogenous and synthetic cannabinoids seem not always identical. Here, we compared the effects of endogenous cannabinoids anandamide (AEA) and synthetic counterparts WIN 55,212-2 (WIN) on synaptic plasticity in hippocampal CA1 region of the anesthetized rats. CB1 blockade by AM281 attenuated high frequency stimulation (HFS)-LTP significantly, but ANA in the micromolar range (1~100μM) also inhibited LTP, whereas ANA with lower concentration (0.1μM) exhibited significant enhancement of LTP. It seemed ANA exerted dual actions on LTP induction. However, WIN potently attenuated basal synaptic transmission and HFS-LTP dose-dependently. Furthermore, the decrease of LTP induced by ANA, but not WIN, could be restored to control level after forskolin application, suggesting the inhibitory potency of ANA on adenylyl cyclase is weaker than WIN. In conclusion, our results reveal some differential effects of endogenous and synthetic cannabinoids in vivo and suggest AEA probably play a more subtle physiological role in the hippocampus than the solely prevention of LTP. | |||
TO cite this article:Wang Wei,Liu Changjin. Differential effects of anandamide and WIN 55,212-2 on hippocampal CA1 long-term potentiation in vivo[OL].[27 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4409272 |
9. Divalent metal transporter 1 upregulation is involved in the 6-hydroxydopamine induced ferrous iron influx | |||
Song Ning ,Jiang Hong,Wang Jun,Xie JunXia | |||
Basic Medicine 27 March 2008 | |||
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Abstract:The reasons underlying the high iron content found in the substantia nigra (SN) of Parkinson’s disease (PD) are largely unknown. Based on our previous studies, we suppose that the newly discovered iron transporter, divalent metal transporter 1 (DMT1), might be involved in this SN iron accumulation process. To investigate this, we first observed the cellular expression of DMT1 in rat SN, both with the iron response element (+IRE) and without the IRE (-IRE) forms. The results showed that both forms of DMT1 were expressed on neurons, astrocytes, and microglia, but not on oligodendrocytes. We further observed the relationship between the increased iron influx and DMT1 expression in 6-hydroxydopamine (6-OHDA) treated C6 cells. 6-OHDA (10μmol/L) caused a significant increase in ferrous iron influx, with the increased expression of DMT1+IRE, both in protein and mRNA levels, while no change was observed for DMT1-IRE. To further clarify that the increased expression of DMT1 was not due to the increased intracellular iron content, C6 cells were overloaded with ferric ammonium citrate (100μg/ml). Decreased expression of both forms of DMT1 was observed. Our data suggest that DMT1 is highly expressed in rat SN in a cellular-specific manner. Increased DMT1+IRE expression is the mechanism behind ferrous iron influx induced by 6-OHDA treatment in C6 cells. This may give some evidence for the involvement of DMT1 in the iron accumulation in PD. | |||
TO cite this article:Song Ning ,Jiang Hong,Wang Jun, et al. Divalent metal transporter 1 upregulation is involved in the 6-hydroxydopamine induced ferrous iron influx[OL].[27 March 2008] http://en.paper.edu.cn/en_releasepaper/content/19795 |
10. Peripheral Iron Dextran Induced Degeneration of Dopaminergic Neurons in Rat Substantia Nigra | |||
Jiang Hong ,Song Ning,Wang Jun ,Ren Li Ying,Xie Jun Xia | |||
Basic Medicine 27 March 2008 | |||
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Abstract:Iron accumulation is considered to be involved in the pathogenesis of Parkinson’s disease. To demonstrate the relationship between peripheral iron overload and dopaminergic neuron loss in rat substantia nigra (SN), in the present study we used fast cyclic voltammetry, tyrosine hydroxylase (TH) immunohistochemistry, Perls’ iron staining, and high performance liquid chromatography-electrochemical detection to study the degeneration of dopaminergic neurons and increased iron content in the SN of iron dextran overloaded animals. The findings showed that peripheral iron dextran overload increased the iron staining positive cells and reduced the number of TH-immunoreactive neurons in SN. As a result, dopamine release and content, as well as its metabolites contents were decreased in caudate putamen. Even more dramatic changes were found in chronic overload group. These results suggest that peripheral iron dextran can increase the iron amount in SN, where excessive iron caused the degeneration of dopaminergic neurons. The chronic iron overload may be more destructive to dopaminergic neurons than the acute iron overload. | |||
TO cite this article:Jiang Hong ,Song Ning,Wang Jun , et al. Peripheral Iron Dextran Induced Degeneration of Dopaminergic Neurons in Rat Substantia Nigra[OL].[27 March 2008] http://en.paper.edu.cn/en_releasepaper/content/19780 |
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