检索结果-南通市图书馆

Effects of amyloid precursor protein peptide APP96-110,alone or with human mesenchymal stromal cells,on recovery after spinal cord injury

引用

Neural Regeneration Research 2022年第6期17卷 1376-1386页

作者： Stuart I.Hodgetts Sarah J.Lovett D.Baron-Heeris A.Fogliani Marian Sturm C.Van den Heuvel Alan R.Harvey School of Human Sciences The University of Western Australia(UWA)PerthWAAustralia Perron Institute for Neurological and Translational Science PerthWAAustralia Cell and Tissue Therapies WA(CTTWA) Royal Perth HospitalPerthWAAustralia Adelaide Medical School Faculty of Health and Medical SciencesThe University of AdelaideAdelaideSAAustralia

Delivery of a peptide(APP96-110),derived from amyloid precursor protein(APP),has been shown to elicit neuroprotective effects following cerebral stroke and traumatic brain injury.In this study,the effect of APP96-110 or a mutant version of this peptide(mAPP96-110)was assessed following moderate(200 kdyn,(2 N))thoracic contusive spinal cord injury(SCI)in adult Nude rats.Animals received a single tail vein injection of APP96-110 or mAPP96-110 at 30 minutes post-SCI and were then assessed for functional improvements over the next 8 weeks.A cohort of animals also received transplants of either viable or non-viable human mesenchymal stromal cells(hMSCs)into the SC lesion site at one week post-injury to assess the effect of combining intravenous APP96-110 delivery with hMSC treatment.Rats were perfused 8 weeks post-SCI and longitudinal sections of spinal cord analyzed for a number of factors including hMSC viability,cyst size,axonal regrowth,glial reactivity and macrophage activation.Analysis of sensorimotor function revealed occasional significant differences between groups using Ladderwalk or Ratwalk tests,however there were no consistent improvements in functional outcome after any of the treatments.mAPP96-110 alone,and APP96-110 in combination with both viable and non-viable hMSCs significantly reduced cyst size compared to SCI alone.Combined treatments with donor hMSCs also significantly increased βIII tubulin^(+),glial fibrillary acidic protein(GFAP^(+))and laminin+expression,and decreased ED1^(+)expression in tissues.This preliminary study demonstrates that intravenous delivery of APP96-110 peptide has selective,modest neuroprotective effects following SCI,which may be enhanced when combined with hMSC transplantation.However,the effects are less pronounced and less consistent compared to the protective morphological and cognitive impact that this same peptide has on neuronal survival and behaviour after stroke and traumatic brain injury.Thus while the efficacy of a particular therapeutic approach in one CNS inju

关键词： amyloid precursor protein cell transplantation combination contusion functional recovery mesenchymal stromal cells neuroprotection regeneration spinal cord injury tissue sparing

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Resveratrol and Sir2 Reverse Sleep and Memory Defects Induced by amyloid precursor protein

引用

Neuroscience Bulletin 2023年第7期39卷 1117-1130页

作者： Yuping Hao Lingzhan Shao Jianan Hou Yan Zhang Yuqian Ma Jinhao Liu Chuan Xu Fujun Chen Li-Hui Cao Yong Ping Bio-X Institutes Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders(Ministry of Education)Shanghai Jiao Tong UniversityShanghai 200240China School of Basic Medical Sciences Capital Medical UniversityBeijing 100069China

Resveratrol(RES),a natural polyphenolic phytochemical,has been suggested as a putative anti-aging molecule for the prevention and treatment of Alzheimer’s disease(AD)by the activation of sirtuin 1(Sirt1/Sir2).In this study,we tested the effects of RES and Sirt1/Sir2 on sleep and courtship memory in a Drosophila model by overexpression of amyloid precursor protein(APP),whose duplications and mutations cause familial AD.We found a mild but significant transcriptional increase of Drosophila Sir2(dSir2)by RES supplementation for up to 17 days in APP flies,but not for 7 days.RES and dSir2 almost completely reversed the sleep and memory deficits in APP flies.We further demonstrated that dSir2 acts as a sleep promotor in Drosophila neurons.Interestingly,RES increased sleep in the absence of dSir2 in dSir2-null mutants,and RES further enhanced sleep when dSir2 was either overexpressed or knocked down in APP flies.Finally,we showed that Aβaggregates in APP flies were reduced by RES and dSir2,probably via inhibiting Drosophilaβ-secretase(dBACE).Our data suggest that RES rescues the APP-induced behavioral deficits and Aβburden largely,but not exclusively,via dSir2.

关键词： Resveratrol Sir2 Sleep amyloid precursor protein β-Secretase Drosophila

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

amyloid precursor protein and growth-associated protein 43 expression in brain white matter and spinal cord tissues in a rat model of experimental autoimmune encephalomyelitis

引用

Neural Regeneration Research 2011年第2期6卷 101-106页

作者： Yizhou Wang Shuang Kou Jingcheng Tang Ping Zhang Qiuxia Zhang Yan Liu Qi Zheng Hui Zhao Lei Wang School of Traditional Chinese Medicine Capital Medical University Beijing 100069 China School of Chemical Biology and Pharmaceutical Sciences CapitalMedical University Beijing 100069 China Pathologic Department Wang Jing Hospital China Academy of Chinese Medical Sciences Beijing 100102 China

Studies have demonstrated that amyloid precursor protein （APP） expression increases in multiple sclerosis tissues during acutely and chronically active stages. To determine the relationship between axonal injury and regeneration in multiple sclerosis, an animal model of experimental autoimmune encephalomyelitis was induced using different doses of myelin basic protein peptide. APP and growth-associated protein 43 （GAP-43）, which is considered a specific marker of neural regeneration, were assessed by western blot analysis. Expression of APP and GAP-43, as well as the correlation between these two proteins, in brain white matter and spinal cord tissues of experimental autoimmune encephalomyelitis rats at different pathological stages was analyzed. Results showed that APP and GAP-43 expression increased during the acute stage and decreased during remission, with a positive correlation between APP and GAP-43 expression in brain white matter and spinal cord tissues. These results suggest that APP and GAP-43 could provide nutritional and protective effects on damaged neurons.

关键词： amyloid precursor protein axonal regeneration central nervous system experimental autoimmune encephalomyelitis growth-associated protein 43

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Two memory associated genes regulated by amyloid precursor protein intracellular domain Novel insights into the pathogenesis of learning and memory impairment in Alzheimer's disease

引用

Neural Regeneration Research 2012年第5期7卷 341-346页

作者： Chuandong Zheng Xi Gu Zhimei Zhong Rui Zhu Tianming Gao Fang Wang Department of Neurobiology School of Basic Medical Sciences Southern Medical University Guangzhou 510515 Guangdong ProvinceChina

In this study, we employed chromatin immunoprecipitation, a useful method for studying the locations of transcription factors bound to specific DNA regions in specific cells, to investigate amyloid precursor protein intracellular domain binding sites in chromatin DNA from hippocampal neurons of rats, and to screen out five putative genes associated with the learning and memory functions. The promoter regions of the calcium/calmodulin-dependent protein kinase II alpha and glutamate receptor-2 genes were amplified by PCR from DNA products immunoprecipitated by amyloid precursor protein intracellular domain. An electrophoretic mobility shift assay and western blot analysis suggested that the promoter regions of these two genes associated with learning and memory were bound by amyloid precursor protein intracellular domain （in complex form）. Our experimental findings indicate that the amyloid precursor protein intracellular domain is involved in the transcriptional regulation of learning- and memory-associated genes in hippocampal neurons. These data may provide new insights into the molecular mechanism underlying the symptoms of progressive memory loss in Alzheimer＇s disease.

关键词： Alzheimer＇s disease amyloid precursor protein amyloid precursor protein intracellular domain chromatin immunoprecipitation gene regulation chromatin DNA

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Impact of Sub-chronic Aluminium-maltolate Exposure on Catabolism of amyloid precursor protein in Rats

引用

Biomedical and Environmental Sciences 2013年第6期26卷 445-452页

作者： LIANG Rui Feng LI Wei Qing WANG Hong WANG Jun Xia NIU Qiao Department of Occupational Health School of Public HealthShanxi Medical University Department of Environmental Health School of Public HealthShanxi Medical University

Objective To investigate the impact of sub-chronic Aluminium-maltolate [Al（mal）s] exposure on the catabolism of amyloid precursor protein （APP） in rats. Methods Forty adult male Sprague-Dawley （SD） rats were randomly divided into five groups： the control group, the maltolate group （7.56 mg/kg BW）, and the Al（mal）s groups （0.27, 0.54, and 1.08 mg/kg BW, respectively）. Control rats were administered with 0.9% normal saline through intraperitoneal （i.p.） injection. Maltolate and Al（mal）s were administered to the rats also through i.p. injections. Administration was conducted daily for two months. Rat neural behavior was examined using open field tests （OFT）. And the protein expressions and their mRNAs transcription related with APP catabolism were studied using enzyme-linked immunosorbent assay （ELISA） and real-time polymerase chain reaction （RT-PCR）. Results The expressions of APP, 13-site APP cleaving enzyme 1 （BACEI） and presenilin-1 （PSi） proteins and their mRNAs transcription increased gradually with the increase of Al（mal）3 doses （P〈0.05）. The enzyme activity of BACEI in the 0.54 and 1.08 mg/kg Al（mal）s groups increased significantly （P〈0.05）. The expression of 8-amyloid protein （AS） 1-40 gradually decreased while the protein expression of A81-42 increased gradually with the increase of Al（mal）s doses （P〈0.05）. Conclusion Result from our study suggested that one of the possible mechanisms that Al（mal）s can cause neurotoxicity is that Al（mal）s can increase the generation of A81-42 by facilitating the expressions of APP, β-, and γ-secretase.

关键词： Aluminium-maltolate amyloid precursor protein 6-amyloid protein Rat

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Estrogen stimulates release of secreted amyloid precursor protein from primary rat cortical neurons via protein kinase C pathway

引用

Acta Pharmacologica Sinica 2005年第2期26卷 171-176页

作者： Sun ZHANG~2,Ying HUANG~2,Yi-chun ZHU~2,Tai YAO~(2,3,4)~2Department of Physiology and Pathophysiology ~3State Key Laboratory for Medical Neurobiology,Shanghai Medical College of FudanUniversity,Shanghai 200032,China Department of Physiology and Pathophysiology Shanghai Medical College of Fudan University Shanghai China State Key Laboratory for Medical Neurobiology Shanghai Medical College of Fudan University Shanghai China

Aim:To investigate the mechanism of the action of estrogen,which stimulates therelease of secreted amyloid precursor protein α(sAPPα)and decreases the gen-eration of amyloid-β protein(Aβ),a dominant component in senile plaques in thebrains of Alzheimer’s disease patients.Methods:Experiments were carried out inprimary rat cortical neurons,and Western blot was used to detect sAPPα in aculture medium and the total amount of cellular amyloid precursor protein(APP)inneurons.Results:17β-Estradiol(but not 17α-estradiol)and β-estradiol 6-(O-carboxymethyl)oxime:BSA increased the secretion of sAPPα and this effect wasblocked by protein kinase C(PKC)inhibitor calphostin C,but not by the classicalestrogen receptor antagonist ICI 182,780.Meanwhile,17β-estradiol did not alterthe synthesis of cellular APP.Conclusion:The effect of 17β-estradiol on sAPPαsecretion is likely mediated through the membrane binding sites,and needs mo-lecular configuration specificity of the ligand.Furthermore,the action of the PKC-dependent pathway might be involved in estrogen-induced sAPPα secretion.

关键词： Alzheimer disease estrogen amyloid precursor protein estrogen receptors protein kinase C

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Inhibiting p38 mitogen-activated protein kinase attenuates cerebral ischemic injury in Swedish mutant amyloid precursor protein transgenic mice

引用

Neural Regeneration Research 2012年第14期7卷 1088-1094页

作者： Liangyu Zou Haiyan Qin Yitao He Heming Huang Yi Lu Xiaofan Chu Department of Neurology Shenzhen People's HospitalSecond Clinical CollegeJinan UniversityShenzhen 518020Guangdong ProvinceChina

Cerebral ischemia was induced using photothrombosis 1 hour after intraperitoneal injection of the p38 mitogen-activated protein kinase （MAPK） inhibitor $B239063 into Swedish mutant amyloid precursor protein （APP/SWE） transgenic and non-transgenic mice. The number of surviving neurons in the penumbra was quantified using Nissl staining, and the activity of p38 MAPKs was measured by western blotting. The number of surviving neurons in the penumbra was significantly reduced in APP/SWE transgenic mice compared with non-transgenic controls 7 days after cerebral ischemia, but the activity of p38 MAPKs was significantly elevated compared with the non-ischemic hemisphere in the APP/SWE transgenic mice. SB239063 prevented these changes. The APP/SWE mutation exacerbated ischemic brain injury, and this could be alleviated by inhibiting p38 MAPK activity.

关键词： cerebral ischemia amyloid precursor protein transgenic Alzheimer＇s disease p38mitogen-activated protein kinase SB239063 neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Divalent cation tolerance protein binds to β-secretase and inhibits the processing of amyloid precursor protein

引用

Neural Regeneration Research 2013年第11期8卷 991-999页

作者： Runzhong Liu Haibo Hou Xuelian Yi Shanwen Wu Huan Zeng State Key Laboratory of Cellular Stress Biology Department of Biomedical Sciences School of Life Sciences Xiamen University Xiamen Maternal and Child Health Hospital

The deposition of amyloid-beta is a pathological hallmark of Alzheimer＇s disease, amyloid-beta is derived from amyloid precursor protein through sequential proteolytic cleavages by β-secretase （beta-site amyloid precursor protein-cleaving enzyme 1） and r-secretase. To further elucidate the roles of beta-site amyloid precursor protein-cleaving enzyme 1 in the development of AIzheimer＇s disease, a yeast two-hybrid system was used to screen a human embryonic brain cDNA library for proteins directly interacting with the intracellular domain of beta-site amyloid precursor protein-cleaving enzyme 1. A potential beta-site amyloid precursor protein-cleaving enzyme 1- interacting protein identified from the positive clones was divalent cation tolerance protein. Immunoprecipitation studies in the neuroblastoma cell line N2a showed that exogenous divalent cation tolerance protein interacts with endogenous beta-site amyloid precursor protein-cleaving enzyme 1. The overexpression of divalent cation tolerance protein did not affect beta-site amyloid precursor protein-cleaving enzyme 1 protein levels, but led to increased amyloid precursor protein levels in N2a/APP695 cells, with a concomitant reduction in the processing product amyloid precursor protein C-terminal fragment, indicating that divalent cation tolerance protein inhibits the processing of amyloid precursor protein. Our experimental findings suggest that divalent cation tolerance protein negatively regulates the function of beta-site amyloid precursor protein-cleaving enzyme 1. Thus, divalent cation tolerance protein could play a protective role in Alzheimer＇s disease.

关键词： neural regeneration brain injury neurodegenerative diseases Alzheimer＇s disease amyloid-betaβ-secretase amyloid precursor protein beta-site amyloid precursor protein-cleaving enzyme 1 interaction amyloid precursor protein C-terminal fragment western blot yeast two-hybridization grants-supported paper neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Inhibition of beta-site amyloid precursor protein-cleaving enzyme and beta-amyloid precursor protein genes in SK-N-SH cells

引用

Neural Regeneration Research 2009年第6期4卷 418-425页

作者： Suqin Gao Lin Sun Enji Han Hongshun Qi Jinbo Feng Shunliang Xu Wen Xia Department of Cerebrovascular Disease Qilu Hospital Shandong University Jinan 250012 Shandong Province China Department of Neurology Second Hospital Shandong University Jinan 250033 Shandong Province China Key Laboratory of Cardiovascular Remodeling and Function Research Ministries of Education and Public Health Jinan 250012 Shandong Province China

BACKGROUND： Previous studies have demonstrated that Piper futokadsura stem selectively inhibits expression of amyloid precursor protein （APP） at the mRNA level. In addition, the piperlonguminine （A） and dihydropiperlonguminine （B） components （1 ： 0.8）, which can be separated from Futokadsura stem, selectively inhibit expression of the APP at mRNA and protein levels. OBJECTIVE： Based on previous findings, the present study investigated the effects of β-site amyloid precursor protein cleaving enzyme （BACE1） and APP genes on the production of β-amyloid peptide 42 （Aβ42） in human neuroblastoma cells （SK-N-SH cells） using small interfering RNAs （siRNAs） and A/B components separated from Futokadsura stem, respectively. DESIGN, TIME AND SETTING： A gene interference-based randomized, controlled, in vitro experiment was performed at the Key Laboratory of Cardiovascular Remodeling and Function Research, Ministries of Education and Public Health, and Institute of Pharmacologic Research, School of Pharmaceutical Science ＆ Department of Biochemistry, School of Medicine, Shandong University between July 2006 and December 2007. MATERIALS： SK-N-SH cells were provided by Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai, China; mouse anti-human BACE1 monoclonal antibody was purchased from R＆D Systems, USA; mouse anti-human APP monoclonal antibody was purchased from Cell Signaling Technology, USA; and horseradish peroxidase （HRP）-conjugated goat anti-mouse IgG was provided by Sigma, USA. METHODS： The human BACE1 cDNA sequence was obtained from NCBI website （www.***.nlm.***.gov/sites/entrez）. Three pairs of siRNAs, specific to human BACE1 gene, were synthesized through the use of Silencer pre-designed siRNA specification, and were transfected into SK-N-SH cells with siPORT NeoFX transfection agent to compare the effects of different concentrations of siRNAs （10-50 nmol/L） on SK-N-SH cells. Futokadsura stem was separated and purified with chemical methods, and the crystal was composed of A/B componen

关键词： Alzheimer＇s disease β-site amyloJd precursor protein cleaving enzyme amyloid precursor protein small interfering RNA piperlonguminine dihydropiperlonguminine Futokadsura stem

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Mutant amyloid precursor protein and presenilin-1 genes effect on ischemia vulnerability via calcium homeostasis disturbance

引用

Neural Regeneration Research 2009年第12期4卷 1049-1054页

作者： Liangyu Zou Xiaofan Chu Haiyan Yin Xuejun Fu Yiguang Rao Gang Li Yi Lu Department of Neurology Shenzhen People's Hospital Second Clinical College Jinan University Shenzhen 518020 Guangdong Province China Intensive Care Unit Guangzhou Red Cross Hospital Fourth Affiliated Hospital Jinan University Guangzhou 510250 Guangdong Province China

BACKGROUND： Previous studies have demonstrated that mutant amyloid precursor protein （APP） or presenilin-1 （PS1） genes increase susceptibility to ischemic brain damage induced by middle cerebral artery occlusion. Possible mechanisms include over-production of beta-amyloid peptide （Aβ）. OBJECTIVE： Because Aβ is over-produced in the APP/PS1 double-transgenic mouse, the present study focused on mechanisms of increased ischemic damage due to mutant APP and PS1 genes by measuring oxidative stress, mitochondrial function, and calcium homeostasis. DESIGN, TIME AND SETTING： The non-randomized, controlled, in vivo and in vitro experiments were performed at the Medical Research Center, Second Clinical College, Jinan University between May and October 2008. MATERIALS： Male APP transgenic mice carrying the mutant 695swe gene and female PS1 transgenic mice carrying the mutant Leu235Pro gene were donated from the University of Hong Kong. SHSY5Y human neureblastoma cells were purchased from ATCC （Manassas, VA, USA）, and Aβ1-42 was obtained from Sigma-Aldrich （St. Louis, MO, USA）. METHODS： APP transgenic mice were mated with PS1 transgenic mice to produce APP/PS1 double-transgenic mice and wildtype littermates mice. The photothrombotic stroke model was induced in six APP/PS1 double-transgenic and 6 wildtype littermates mice. SHSY5Y human neuroblastoma cells were cultured in vitro, and were divided into 4 groups： Aβ group, cells were exposed to 5 pmol/L Aβ for 24 hours; oxygen-glucose deprivation （OGD） group, cells were exposed to OGD for 1 hour after treatment with sterile, ultra-pure water for 24 hours; OGD＋Aβ group, cells were exposed to OGD and Aβfor 1 hour after treatment with 5 pmol/L Aβ for 24 hours; sham control group： cells were exposed to sterile, ultra-pure water for 25 hours. OGD was achieved by exposing the cells to glucose-free DMEM and placing the cells in an anaerobic chamber flushed with 5% CO2 and 95% N2 （v/v） at 37 ℃ for 1 hour. MAIN OUTCOME MEASURES： TTC staining was used to measure infarct volume 7 days after

关键词： amyloid precursor protein presenilin-1 cerebral ischemia calcium d

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：