检索结果-南通市图书馆

Exosome-transported IncRNA H19 regulates insulin-like growth factor-1 via the H19/let-7a/insulin-like growth factor-1 receptor axis in ischemic stroke

引用

Neural Regeneration Research 2023年第6期18卷 1316-1320页

作者： Jue Wang Bin Cao Yan Gao Yu-Hua Chen Juan Feng Department of Neurology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Developmental Cell Biology Key Laboratory of Cell BiologyMinistry of Public Healthand Key Laboratory of Medical Cell BiologyMinistry of EducationChina Medical UniversityShenyangLiaoning ProvinceChina

LncRNA(long non-coding RNA) H19 is a transcript of the H19 gene that is expressed during *** previously discove red a role for circular lncRNA H19 in the onset and prognosis of cerebral ischemic *** this study,we used serum from patients with ischemic stroke,and mouse and cell culture models to elucidate the roles of plasma and neuronal exosomes in the regulatory effect of lncRNA H19 on insulin-like growth factor-1 and its mechanism in ischemic stroke,using western blotting,quantitative real-time polymerase chain reaction,and enzyme-linked immunosorbent *** exosomal IncRNA H19 was negatively associated with blood levels of insulin-like growth factor-1 in samples from patients with cerebral ischemic *** a mouse model,levels of exosomal IncRNA H19 were positively correlated with plasma and cerebral lncRNA *** a cell co-culture model,we confirmed that IncRNA H19 was transported from neuro ns to astrocytes by exosomes to induce downregulation of insulin-like growth factor-1 through the H19/let-7 a/insulin-like growth factor-1 receptor *** study provides the first evidence for the transpo rtation of IncRNA H19 by exosomes and the relationship between IncRNA H19 and insulinlike growth factor-1.

关键词： cerebral ischemia exosomes H19 insulin-like growth factor-1 insulin-like growth factor 1 receptor ischemic stroke long non-coding RNA

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

RNA interference affects tumorigenicity and expression of insulin-like growth factor-1,insulin-like growth factor-1 receptor,and basic fibroblast growth factor-2 in rat C6 glioma cells

引用

Neural Regeneration Research 2009年第8期4卷 597-605页

作者： Wanli Dong Jin Hu Shaoyan Hu Yuanyuan Wang Juean Jiang Youxin Jin Department of Neurology First Affiliated Hospital of Soochow University Suzhou 215006 Jiangsu Province China Sixth People's Hospital of Shanghai Jiao Tong University Shanghai 200233 China State Key Laboratory of Molecular Biology Institute of Biochemistry Chinese Academy of Sciences Shanghai 200031 China

BACKGROUND： Human gliomas are more likely to express basic fibroblast growth factor-2 （FGF-2） insulin-like growth factor-1（IGF-1）, and IGF-1 receptor （IGF-1R） than normal brain tissue. These factors activate signal transduction systems of Ras/MAPK and PI3K/Akl, which promote glioma growth. OBJECTIVE： To utilize RNA interference （RNAi） technique to down-regulate FGF-2, IGF-1, and IGF-1R gene expression, and to investigate the effects of these genes on rat C6 glioma cells, as well as the feasibility of RNAi for treating glioma. DESIGN, TIME AND SETTING： This neurooncological, randomized, controlled, in vivo and in vitro experiment, which used RNAi methodology, was performed at the Laboratory of Molecular Biology, Institute of Biochemistry, Chinese Academy of Sciences between August 2005 and February 2008. MATERIALS： Rat C6 cell lines were purchased from Shanghai Institute of Cellular Biology Affiliated to Chinese Academy of Sciences. Small interfering RNA （siRNA） was synthesized by Shanghai GenePharma. Anti-IGF-1, anti-IGF-1R, anti-FGF-2, anti-mouse and anti-rabbit IgG G1-HRP antibodies were provided by Santa Cruz Biotechnology, USA. Four to six week-old BALB/c nude mice were purchased from the Laboratory Animal Center, Chinese Academy of Sciences. METHODS： C6 glioma cells were transfected with siRNA, which was chemically synthesized in vitro to correspond to endogenous FGF-2, IGF-1, and IGF-1R genes. The inhibition ratio of targeting mRNA expression was detected by semiquantitative RT-PCR, and protein expression was determined by Western blot analysis. C6 glioma cell proliferation was observed using a growth curve C6 glioma cell apoptosis rate and cell cycle were detected by flow cytometry. C6 glioma cell growth regression was observed by transwell migration assay. In addition, nude mouse subcutaneous tumor models were used in this study. For studying the anti-tumor effects of IGF-1 and IGF-1R siRNA, two blank control groups, with six mice each, were set up： A （2.5 μ

关键词： small interference RNA basic fibroblast growth factor-2 insulin-like growth factor 1 insulin-like growth factor 1 receptor C6 glioma cell line

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

An updated review of gastric cancer in the next-generation sequencing era:Insights from bench to bedside and vice versa

引用

World Journal of Gastroenterology 2014年第14期20卷 3927-3937页

作者： Hiroyuki Yamamoto Yoshiyuki Watanabe Tadateru Maehata Ryo Morita Yoshihito Yoshida Ritsuko Oikawa Shinya Ishigooka Shun-ichiro Ozawa Yasumasa Matsuo Kosuke Hosoya Masaki Yamashita Hiroaki Taniguchi Katsuhiko Nosho Hiromu Suzuki Hiroshi Yasuda Yasuhisa Shinomura Fumio Itoh Division of Gastroenterology and Hepatology Department of Internal MedicineSt. Marianna University School of Medicine Division of Cancer Cell Research Institute of Medical ScienceUniversity of Tokyo Department of Gastroenterology Rheumatology and Clinical ImmunologySapporo Medical University School of Medicine Department of Molecular Biology Sapporo Medical University School of Medicine

Gastric cancer(GC)is one of the most common malignancies and remains the second leading cause of cancer-related death *** is an increasing understanding of the roles that genetic and epigenetic alterations play in *** studies using nextgeneration sequencing(NGS)have revealed a number of potential cancer-driving genes in ***-exome sequencing of GC has identified recurrent somatic mutations in the chromatin remodeling gene ARID1A and alterations in the cell adhesion gene FAT4,a member of the cadherin gene *** in chromatin remodeling genes(ARID1A,MLL3 and MLL)have been found in 47%of ***-genome sequencing and whole-transcriptome sequencing analyses have also discovered novel alterations in *** studies of cancer epigenetics have revealed widespread alterations in genes involved in the epigenetic machinery,such as DNA methylation,histone modifications,nucleosome positioning,noncoding RNAs and *** advances in molecular research on GC have resulted in the introduction of new diagnostic and therapeutic strategies into clinical *** antihuman epidermal growth receptor 2(HER2)antibody trastuzumab has led to an era of personalized therapy in *** addition,ramucirumab,a monoclonal antibody targeting vascular endothelial growth factor receptor(VEGFR)-2,is the first biological treatment that showed survival benefits as a single-agent therapy in patients with advanced GC who progressed after firstline *** NGS to systematically identify gene alterations in GC is a promising approach with remarkable potential for investigating the pathogenesis of GC and identifying novel therapeutic targets,as well as useful *** this review,we will summarize the recent advances in the understanding of the molecular pathogenesis of GC,focusing on the potential use of these genetic and epigenetic alterations as diagnostic biomarkers and novel therapeutic targets.

关键词： Next-generation sequencing Microsatellite instability MicroRNA Epigenetic field defect Gastric washes insulin-like growth factor 1 receptor

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

Enriched gestation activates the IGF pathway to evoke embryo-adult benefits to prevent Alzheimer’s disease

引用

Translational Neurodegeneration 2019年第1期8卷 94-110页

作者： Enjie Liu Qiuzhi Zhou Ao-Ji Xie Mengzhu Li Shujuan Zhang Hezhou Huang Zhenyu Liuyang Yali Wang Bingjin Liu Xiaoguang Li Dongsheng Sun Yuping Wei Xiaochuan Wang Qun Wang Dan Ke Xifei Yang Ying Yang Jian-Zhi Wang Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Co-innovation Center of Neuroregeneration Nantong UniversityNantong 226000China Key Laboratory of Modern Toxicology of Shenzhen Shenzhen Centre for Disease Control and Prevention8 Longyuan RoadShenzhen 518055China Department of Pathology the First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052China

Background:Building brain reserves before dementia onset could represent a promising strategy to prevent Alzheimer’s disease(AD),while how to initiate early cognitive stimulation is *** that the immature brain is more sensitive to environmental stimuli and that brain dynamics decrease with ageing,we reasoned that it would be effective to initiate cognitive stimulation against AD as early as the fetal ***:After conception,maternal AD transgenic mice(3×Tg AD)were exposed to gestational environment enrichment(GEE)until the day of *** cognitive capacity of the offspring was assessed by the Morris water maze and contextual fear-conditioning tests when the offspring were raised in a standard environment to 7 months of *** blotting,immunohistochemistry,real-time PCR,immunoprecipitation,chromatin immunoprecipitation(ChIP)assay,electrophysiology,Golgi staining,activity assays and sandwich ELISA were employed to gain insight into the mechanisms underlying the beneficial effects of GEE on embryos and 7–10-month-old adult ***:We found that GEE markedly preserved synaptic plasticity and memory capacity with amelioration of hallmark pathologies in 7–10-m-old AD *** beneficial effects of GEE were accompanied by global histone hyperacetylation,including those at bdnf promoter-binding regions,with robust BDNF mRNA and protein expression in both embryo and progeny *** increased insulin-like growth factor 1(IGF1)and activated its receptor(IGF1R),which phosphorylates Ca^(2+)/calmodulin-dependent kinase IV(CaMKIV)at tyrosine sites and triggers its nuclear translocation,subsequently upregulating histone acetyltransferase(HAT)and BDNF *** upregulation of IGF1 mimicked the effects of GEE,while IGF1R or HAT inhibition during pregnancy abolished the GEE-induced CaMKIV-dependent histone hyperacetylation and BDNF ***:These findings suggest that activation of IGF1R/CaMKIV/HAT/BDNF signal

关键词： Alzheimer’s offspring Brain-derived neurotrophic factor Gestational environment enrichment Histone acetyltransferase insulin-like growth factor 1 receptor

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

insulin-like growth factor-binding protein-3 inhibits IGF-1-induced proliferation of human hepatocellular carcinoma cells

引用

中国药理学与毒理学杂志 2017年第10期31卷 966-966页

作者： Yang MA Chen-chen HAN Yi-fan LI Yang WANG Wei WEI Institute of Clinical Pharmacology Anhui Medical UniversityKey Laboratory of Anti-inflammatory and Immune MedicineMinistry of EducationAnhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine

OBJECTIVE Basic fibroblast growth factor(b FGF)and platelet-derived growth factor(PDGF)produced by hepatocellular carcinoma(HCC)cells are responsible for the cell *** evidence shows that insulin-like growth factor-binding protein-3(IGFBP-3)suppresses HCC cell proliferation in both IGF-dependent and independent *** present study is to investigate whether treatment with exogenous IGFBP-3 inhibits bF GF and PDGF production and the cell proliferation of HCC *** Cell Counting Kit 8 assay were designed to detect HCC cell proliferation,transcription factor early growth response-1(EGR1)involving in IGFBP-3 regulation of b FGF and PDGF were detected by RT-PCR and Western blot *** blot assay was adopted to detect the IGFBP-3 regulating insulin-like growth factor 1 receptor(IGF-1R)signaling *** The present study demonstrates that IGFBP-3 suppressed IGF-1-induced b FGF and PDGF expression while it does not affect their expression in the absence of *** delineate the underlying mechanism,Western-blot and RT-PCR assays confirmed that the transcription factor early growth response protein 1(EGR1)is involved in IGFBP-3 regulation of b FGF and ***-3 inhibition of type 1 insulin-like growth factor receptor(IGF1R),ERK and AKT activation is ***,transient transfection with constitutively activated AKT or MEK partially blocks the IGFBP-3 inhibition of EGR1,b FGF and PDGF *** In conclusion,these findings suggest that IGFBP-3suppresses transcription of EGR1 and its target genes b FGF and PDGF through inhibiting IGF-1-dependent ERK and AKT *** demonstrates the importance of IGFBP-3 in the regulation of HCC cell proliferation,suggesting that IGFBP-3 could be a target for the treatment of HCC.

关键词： insulin-like growth factor-binding protein-3 early growth response-1 insulin-like growth factor 1 receptor cell proliferation

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

GPER is involved in the anti-inflammatory effects of genistein in BV2 microglial cells

GPER is involved in the anti-inflammatory effects of geniste...

引用

中国神经科学学会第十二届全国学术会议

作者： Zhong-Rui DU Liang-Jie YUAN Wen-Fang CHEN Department of Physiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders Medical College of Qingdao University

Objective Genistein is an isoflavonoid phytoestrogen extracted from leguminous plants exerting both estrogen agonist and antagonist activities. The present study hypothesized that the anti-inflammatory effects of genistein against lipopolysaccharide（LPS）-induced BV2 microglial activation might be mediated by membrane estrogen receptor（G-protein coupled estrogen receptor, GPER）. Methods The anti-inflammatory effects of genistein were investigated in LPS-induced microglial activation in murine BV2 cells. G1, the specific agonist of GPER, was used as a positive control. The pharmacological blockade and lentivirus-mediated si RNA knockdown of GPER were used to study the underlying mechanism. Results Genistein mimicked the effects of G1 treatment by inhibiting the LPS-induced gene expressions of inflammatory cytokines, including TNF-a, IL-1b, COX-2 and iNOS in BV2 microglial cells. Pretreatment with GPER antagonist G15 or si RNA knockdown of GPER could significantly block the anti-inflammatory effects of genistein and G1. Furthermore, pretreatment with G15 could also block the inhibitory effects of genistein on LPS-induced phosphorylation of JNK, p38, ERK and IkB. Conclusion Genistein exerts antin-inflammatory effects in BV2 microglial cells possibly by the activating GPER.

关键词： genistein G protein-coupled estrogen receptor insulin-like growth factor 1 receptor microglia

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

GPER and IGF-1R mediate the anti-inflammatory effect of genistein against lipopolysaccharide-induced nigrostriatal injury

GPER and IGF-1R mediate the anti-inflammatory effect of geni...

引用

2019中国生理学会学术年会暨张锡钧基金第十五届全国青年优秀生理学学术论文交流会及第十三届全国青年生理学工作者学术会议

作者：张梅 Zhong-Rui Du Wen-Fang Chen Department of Physiology and Pathophysiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological DisordersSchool of Basic MedicineQingdao University

Objective Neuroinflammation plays an important role in the pathogenesis of Parkinson’s disease(PD).The present study was designed to investigate the anti-inflammatory and neuroprotective mechanism of genistein in LPS-induced PD rat *** LPS was injected into the substantia nigra to establish a rat inflammatory model of *** dopamine(DA) content in the striatum was studied by *** numbers of TH-ir neurons and the activation of microglia in the SNpc were detected by *** inflammatory factors protein expressions were detected by western blot and *** Genistein pretreatment could ameliorate the apomorphine-induced rotational behavior in LPS-induced inflammatory PD rat *** attenuated LPS-induced decrease of the contents of DA and its metabolites in striatum as well as the loss of TH-IR neurons in the lesioned side of *** GPER antagonist G15 or IGF-1 R antagonist JB-1 blocked the neuroprotective effects of ***, genistein significantly inhibited LPS-induced microglial activation and production of TNF-α, IL-1β, iNOS and *** of GPER or IGF-1 R by G15 or JB1 could attenuate the anti-inflammatory effects of ***, genistein treatment could inhibit the LPS-induced activation of NF-κB and MAPKs signaling pathways in the lesioned side of SN, which could also be blocked by G15 or *** Genistein inhibits microglial inflammatory responses and protects nigral dopaminergic neurons via GPER and IGF-1 R signaling pathways.

关键词： genistein G protein-coupled estrogen receptor insulin-like growth factor 1 receptor neuroinflammation Parkinson’s disease

来源： cnki会议评论

在线全文

cnki会议

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

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

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：