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Altered Wnt Signaling Pathway in Cognitive Impairment Caused by Chronic Intermittent Hypoxia： Focus on glycogen synthase kinase-3β and β-catenin

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Chinese Medical Journal 2016年第7期129卷 838-845页

作者： Yue-Ying Pan Yan Deng Sheng Xie Zhi-Hua Wang YuWang Jie Ren Hui-Guo Liu Department of Respiratory and Critical Care Medicine Tongji Hospital Tongli Medical College Huazhong University of Science and Technology Key Laboratory of Respiratory Disease of the Ministry of Health Wuhan Hubei 430030 China

Background： Cognitive impairment is a severe complication caused by obstructive sleep apnea （OSA）. The mechanisms of causation are still unclear. The Wntβ-catenin signaling pathway is involved in cognition, and abnormalities in it are implicated in neurological disorders. Here, we explored the Wntβ-catenin signaling pathway abnormalities caused by chronic intermittent hypoxia （CIH）, the most characteristic pathophysiological component of OSA. Methods： We divided 32 4-week-old male C57/BL mice into four groups of eight each： a CIH ＋ normal saline （NS） group, CIH ＋ LiCI group, sham CIH ＋ NS group, and a sham CIH ＋ LiCI group. The spatial learning performance of each group was assessed by using the Morris water maze （MWM）. Protein expressions of glycogen synthase kinase-β （GSK-β） and β-catenin in the hippocampus were examined using the Western blotting test. EdU labeling and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining methods were used, respectively, to determine the proliferation and apoptosis of neurons in the hippocampal dentate gyrus region. Results： Mice exposed to CIH showed impaired spatial learning performance in the MWM, including increased mean escape latencies to reach the target platform, decreased mean times passing through the target platform and mean duration in the target quadrant. The GSK-313 activity increased, and expression of β-catenin decreased significantly in the hippocampus of the CIH-exposed mice. Besides, CIH significantly increased hippocampal neuronal apoptosis, with an elevated apoptosis index. Meanwhile, LiCI decreased the activity of GSK-β and increased the expression of β-catenin and partially reversed the spatial memory deficits in MWM and the apoptosis caused by CIH. Conclusions： Wntβ-catenin signaling pathway abnormalities possibly play an important role in the development of cognitive deficits among mice exposed to CIH and that LiCI might attenuate CIH-induced cognitive impairment via Wntβ-c

关键词： β-catenin Chronic Intermittent Hypoxia Cognition glycogen synthase kinase-3β Hippocampus Obstructive SleepApnea

Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2012年第19期7卷 1507-1512页

作者： Bo Zhao Wenwei Gao Jiabao Hou Yang Wu Zhongyuan Xia Department of Anesthesiology Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China Department of Intensive Care Unit Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China

The present study established global brain ischemia using the four-vessel occlusion method. Following three rounds of reperfusion for 30 seconds, and occlusion for 10 seconds, followed by reperfusion for 48 hours, infarct area, the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced. However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning. Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

关键词： cerebral ischemia/reperfusion glycogen synthase kinase-3β ischemic postconditioning ischemicpreconditioning apoptosis neural regeneration

Cornel iridoid glycoside induces autophagy to protect against tau oligomer neurotoxicity induced by activation of glycogen synthase kinase-3β

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Cornel iridoid glycoside induces autophagy to protect agains...

1-methyl-4-phenylpyridinium ion induces endoplasmic reticulum stress through glycogen synthase kinase-3 beta activation in PC12 cells

2019全国老年痴呆与认知障碍相关疾病学术大会

作者： YANG Cui-cui LI Xue-lian ZHANG Li LI Ya-li LI Lin ZHANG Lan Department of Pharmacy Xuanwu Hospital of Capital Medical UniversityBeijing Institute for Brain DisordersBeijing Engineering Research Center for Nerve System DrugsKey Laboratory for Neurodegenerative Diseases of Ministry of Education Key Laboratory for Basic Pharmacology of Ministry of Education Zunyi Medical College

Tau oligomers are the etiologic molecules of Alzheimer disease(AD),and correlate strongly with neuronal loss and exhibit *** evidence indicates that small tau oligomers are the most relevant toxic aggregate *** aim of the present study was to investigate the mechanisms of cornel iridoid glycoside(CIG) on tau oligomers and cognitive *** injected wortmannin and GF-109203 X(WM/GFX,200 μmol·L each) into the lateral ventricles to induce tau oligomer and memory impairment in *** orally administered with CIG at 60 and 120 mg·kg-1 per day for 14 d,CIG decreased the escape latency in Morris water maze *** also found that CIG restored the expression of presynaptic p-synapsin,synaptophysin,and postsynaptic density-95(PSD-95) decreased by WM/GFX in rat *** reduced the accumulation of tau oligomers in the brain of WM/GFX rats and in cells transfected with wild type glycogen synthase kinase-3β(wtGSK-3β).In addition,CIG up-regulated the levels of ATG7,ATG12,Beclin-1,and LC3 II in vivo and in vitro,suggesting the restoration of autophagy *** results suggest that CIG could ameliorate memory deficits and regulate memory-associated synaptic proteins through the clearance of tau oligomers ***,CIG clears tau oligomers by restoring autophagy function.

关键词： cornel iridoid glycoside autophagy tau oligomer glycogen synthase kinase-3β

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Neural Regeneration Research 2011年第11期6卷 805-810页

作者： Shengdong Wang Fucheng Luo Yan Chen Lei Qi Jie Bai College of Life Science and Technology Kunming University of Science and Technology Kunming 650224 Yunnan Province China

1-methyl-4-phenylpyridinium ion （MPP^＋） induces endoplasmic reticulum stress and activates caspase-12 in PC12 cells, leading to neuronal apoptosis. However, the underlying molecular mechanism remains unknown. The present study investigated the regulatory effects of nerve growth factor （Akt activator） and lithium chloride （glycogen synthase kinase-3β inhibitor） on the endoplasmic reticulum stress signaling pathway. The results revealed that MPP＋ induced expression of Bip and C/EBP homologous protein. The upregulation of Bip and C/EBP homologous protein, as well as the decreased pro-caspase-12 level induced by MPP^＋ were inhibited by pretreatment of the nerve growth factor or lithium chloride. These results suggest that the phosphatidylinositol 3 kinase-Aktglycogen synthase kinase-3β pathway is involved in MPP-induced endoplasmic reticulum stress.

关键词： Parkinson's disease 1-methyl-4-phenylpyridinium ion endoplasmic reticulum stress glycogen synthase kinase-3β

High-frequency (50 Hz) electroacupuncture ameliorates cognitive impairment in rats with amyloid beta 1–42-induced Alzheimer＇s disease

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Neural Regeneration Research 2018年第10期13卷 1833-1841页

作者： Chao-Chao Yu Ying Wang Feng Shen Li-Hong Kong Ya-Wen Wang Hua Zhou Lei Tang Hubei University of Chinese Medicine WuhanHubei ProvinceChina Department of Acupuncture and Moxibustion College of Acupuncture and OrthopedicsHubei University of Chinese MedicineWuhanHubei ProvinceChina Department of Rehabilitation Wuhan Central Hospital Affiliated to Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina

Acupuncture has been shown to ameliorate cognitive impairment of Alzheimer’s *** and stimulation frequency influence the therapeutic effect of *** models of Alzheimer’s disease were established by injecting amyloid beta 1–42（Aβ_（1–42））into the bilateral lateral *** at 2,30,and 50 Hz was carried out at Baihui（GV20;15°obliquely to a depth of 2mm）and Shenshu（BL23;perpendicularly to 4–6 mm depth）,once a day for 20 minutes（each）,for 15 days,taking a break every 7 *** Morris water maze test was conducted to assess the learning and *** expression levels of glycogen synthase kinase-3β（GSK-3β）,p Ser9-GSK-3β,p Tyr216-GSK-3β,amyloid precursor protein and Aβ_（1–40） in the hippocampus were determined by western blot *** demonstrated that electroacupuncture treatment at different frequencies markedly improved learning and memory ability,increased synaptic curvatures,decreased the width of synaptic clefts,thickened postsynaptic densities,and downregulated the expression of GSK-3β,amyloid precursor protein,and Aβ_（1–40）.pSer9-GSK-3βexpression markedly decreased,while p Tyr216-GSK-3βexpression ***-frequency（50 Hz）electroacupuncture was more effective than low（2 Hz）or medium-frequency（30 Hz）*** conclusion,electroacupuncture treatment exerts a protective effect against Aβ_（1–42）-induced learning and memory deficits and synapse-ultrastructure impairment via inhibition of GSK-3β***,high-frequency electroacupuncture was the most effective therapy.

关键词： nerve regeneration electroacupuncture different frequencies Alzheimer's disease cognitive impairment hippocampus glycogen synthase kinase-3β synaptic curvatures width of synaptic cleft postsynaptic density Baihui(GV20) Shenshu(BL23) neural regeneration

The mechanism of Naringin-enhanced remyelination after spinal cord injury

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Neural Regeneration Research 2017年第3期12卷 470-477页

作者： Wei Rong Yong-wei Pan Xu Cai Fei Song Zhe Zhao Song-hua Xiao Cheng Zhang Department of Orthopedics Beijing Tsinghua Changgung HospitalMedical CenterTsinghua UniversityBeijing Key Laboratory of Bioelectromagnetism Beijing Key Laboratory of Bioelectromagnetism Institute of Electrical EngineeringChinese Academy of Sciences

Our previous study revealed that intragastric administration of naringin improved remyelination in rats with spinal cord injury and promoted the recovery of neurological function of the injured spinal *** study sought to reveal the mechanisms by which naringin improves oligodendrocyte precursor cell differentiation and maturation,and promotes *** cord injury was induced in rats by the weight-drop *** was intragastrically administered daily（20,40 mg/kg） for 4 weeks after spinal cord injury *** assessment,histopathological staining,immunofluorescence spectroscopy,ultrastructural analysis and biochemical assays were *** treatment remarkably mitigated demyelination in the white matter,increased the quality of myelinated nerve fibers and myelin sheath thickness,promoted oligodendrocyte precursor cell differentiation by upregulating the expression of NKx2.2 and 2′3′-cyclic nucleotide 3′-phosphodiesterase,and inhibited β-catenin expression and glycogen synthase kinase-3β（GSK-3β） *** findings indicate that naringin treatment regulates oligodendrocyte precursor cell differentiation and promotes remyelination after spinal cord injury through the β-catenin/GSK-3β signaling pathway.

关键词： nerve regeneration spinal cord injury naringin remyelination oligodendrocyte precursor cells oligodendrocytes β-catenin glycogen synthase kinase-3β NKx2.2 2',3'-cyclic nucleotide 3'-phosphodiesterase behavioral assessment neural regeneration

Combined treatment with valproic acid and estrogen has neuroprotective effects in ovariectomized mice with Alzheimer’s disease

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Neural Regeneration Research 2021年第10期16卷 2078-2085页

作者： Yan-Zhen Li Yuan-Jie Liu Wei Zhang Shi-Fang Luo Xin Zhou Gui-Qiong He Chongqing Key Laboratory of Neurobiology Chongqing Medical UniversityChongqingChina Department of Anatomy Chongqing Medical UniversityChongqingChina Department of Galactophore Chongqing University Cancer HospitalChongqingChina

Postmenopausal women with Alzheimer’s disease exhibit dramatically reduced sensitivity to estrogen replacement therapy,which is though to be related to an estrogen receptor(ER)α/ERβratio imbalance arising from a significantly decreased level of ERs of the *** aim of our study was to investigate whether valproic acid(VPA)can enhance the beneficial effects of estrogen on cognitive function through restoration of ERαand ERβexpression in the *** removed the ovaries of female APP/PS1 mice to simulate the low estrogen levels present in postmenopausal women and then administered VPA(30 mg/kg,intraperitoneal injection,once daily),17β-estradiol(E2)(2.4μg,intraperitoneal injection,once daily),liquiritigenin(LG)(50μg/kg,intragastric infusion,once daily),VPA+E2,or VPA+LG for 4 successive *** with treatment with a single drug,treatment with VPA+E2 or VPA+LG significantly increased the level of glycogen synthase kinase 3β,increased the expression of estrogen receptorα,reduced the expression of small ubiquitin-like modifiers,and increased the level of estrogen receptorβ.This resulted in enhanced sensitivity to estrogen therapy,reduced amyloidβaggregation,reduced abnormal phosphorylation of the tau protein,reduced neuronal loss,increased dendritic spine and postsynaptic density,and significantly alleviated memory loss and learning impairment in Alzheimer’s *** study was approved by the Chongqing Medical University Animal Protection and Ethics Committee,China on March 6,2013.

关键词： 17β-estradiol amyloidβ dementia estrogen receptorα estrogen receptorβ glycogen synthase kinase-3β liquiritigenin menopause neuron loss tau

Role of Microtubule-associated Protein Tau Phosphorylation in Alzheimer's Disease

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2017年第3期37卷 307-312页

作者：马荣红张瑶洪小月张俊菲王建枝刘恭平 Department of Laboratory Medicine Union Hospital Tongji Medical College Huazhong University of Science and Technology Department of Endocrinology Liyuan Hospital Key Laboratory of Hubei Province for Neurological Disorders Key Laboratory of Ministry of Education of China for Neurological Disorders Tongji Medical College Huazhong University of Science and Technology Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain Science Key Laboratory of Hubei Province and Ministry of Education of China for Neurological Disorders Tongji Medical College Huazhong University of Science and Technology

As a major microtubule-associated protein, tau plays an important role in promoting microtubule assembly and stabilizing microtubules. In Alzheimer’s disease(AD) and other tauopathies, the abnormally hyperphosphorylated tau proteins are aggregated into paired helical filaments and accumulated in the neurons with the form of neurofibrillary tangles. An imbalanced regulation in protein kinases and protein phosphatases is the direct cause of tau hyperphosphorylation. Among various kinases and phosphatases, glycogen synthase kinase-3β(GSK-3β) and protein phosphatase 2A(PP2A) are the most implicated. Accumulation of the hyperphosphorylated tau induces synaptic toxicity and cognitive impairments. Here, we review the upstream factors or pathways that can regulate GSK-3β or PP2A activity mainly based on our recent findings. We will also discuss the mechanisms that may underlie tau-induced synaptic toxicity.

关键词： Alzheimer's disease tau glycogen synthase kinase-3β protein phosphatase 2A synaptic toxicity

Unilateral amyloid-β25-35 injection into the rat amygdala increases the expressions of aberrant tau phosphorylation kinases

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Chinese Medical Journal 2010年第10期123卷 1311-1314页

作者： HUANG Jing CHEN Yu-juan BIAN Wei-hong YU Jing ZHAO Yu-wu LIU Xue-yuan Department of Neurology Shanghai 10th People's Hospital Tongji University School of Medicine Shanghai 200072 China Department of Neurology Shanghai Sixth People's Hospital Shanghai 200233 China

Background Neuropathologically, Alzheimer disease （AD） is characterized by the presence of extracellular plaques enriched in β-amyloid peptides; however, the mechanism by which it results in the neurotoxicity is uncertain. The purpose of this study was to investigate whether it would prompt the progress of Alzheimer disease via enhancement of aberrant phosphorylated tau that results from its increased kinase gene expression. Methods Twenty-four male rats were divided into three groups, and each group had 8 rats： control, sham-operated, and Aβ25-35 injected AD model groups. AD rat models were created by unilateral injections of Aβ25-35 into the amygdala. The hyperphosphorylated tau protein was estimated by immunohistochemistry with paired helical filament-1 （PHF-1） antibody and paired helical filament-tau （AT8） antibody. The expressions of glycogen synthase kinase-3β （GSK-3β） and p38 mitogen-activated protein kinase （P38MAPK） mRNA were observed by in situ hybridization. Results Compared with the control and sham-operated groups, the evaluation of paired AT8 and paired helical filament-1 （PHF-1） in the cortexes and hippocampus of the AD model group showed the numbers of AT8 and PHF-1 positive cells, as well as the optical density （OD） values of the proteins were significantly higher （AT8： in CA2： 0.318±0.037 vs. 0.135±0.028, 0.136±0.031; in frontal cortex： 0.278±0.040 vs. 0.130±0.028, 0.190±0.037. PHF-1 ： in CA2： 0.386±0.034 vs. 0.139±0.010, 0.193±0.041; in frontal cortex： 0.395±0.050 vs. 0.159±0.030, 0.190±0.044, respectively, P 〈0.01）; the number of GSK-3β mRNA and P38MAPK mRNA positive cells of the AD model group, as well as the OD values, also increased significantly in the cortexes, hippocampus （GSK-3β-mRNA： in CA2：0.384±0.012 vs. 0.190±0.015, 0.258±0.064; in frontal cortex： 0.398±0.018 vs. 0.184±0.031, 0.218±0.049. P38MAPK mRNA： in CA2：0.409±0.038 vs. 0.161±0.041, 0.189±0.035; in frontal cortex： 0.423±0.070 vs. 0.160±0.032, 0.203±0.053, respectively, P 〈0.01）. C

关键词： Alzheimer disease β-amyloid tau proteins glycogen synthase kinase-3β P38 mitogen-activated protein kinase