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Inactivation of ERK1/2-CREB Pathway Is Implicated in MK801-induced Cognitive Impairment

Current medical science 2023年第1期43卷 13-21页

作者： Cui-ping GUO Wen-sheng Li Yi LIU Yacoubou Abdoul Razak Mahaman Bin ZHANG jian-zhi wang Rong LIU Hong-lian LI Xiao-chuan wang Xiang GAO Central laboratory Scientific Research DepartmentRenmin Hospital of Wuhan UniversityWuhan430060China Co-innovation Center of Neuroregeneration Nantong UniversityNantong226001China department of pathophysiology School of Basic MedicineKey Laboratory of Education Ministry/Hubei Province of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Shenzhen huazhong university of science and technology Research Institute Shenzhen518000China

Objective Schizophrenia(SZ)is associated with cognitive impairment,and it is known that the activity of cAMP response element binding protein(CREB)decreases in the brain of SZ *** previous study conducted by the investigators revealed that the upregulation of CREB improves the MK801-related SZ cognitive *** present study further investigates the mechanism on how CREB deficiency is associated with SZ-related cognitive *** MK-801 was used to induce SZ in *** blotting and immunofluorescence were performed to investigate CREB and the CREB-related pathway implicated in MK801 *** long-term potentiation and behavioral tests were performed to assess the synaptic plasticity and cognitive impairment,*** The phosphorylation of CREB at Ser133 decreased in the hippocampus of SZ ***,among the upstream kinases of CREB,merely ERK1/2 was downregulated,while CaMKII and PKA remained unchanged in the brain of MK801-related SZ *** inhibition of ERK1/2 by PD98059 reduced the phosphorylation of CREB-Ser133,and induced synaptic dysfunction in primary hippocampal ***,the activation of CREB attenuated the ERK1/2 inhibitor-induced synaptic and cognitive *** These present findings partially suggest that the deficiency of the ERK1/2-CREB pathway is involved in MK801-related SZ cognitive *** activation of the ERK1/2-CREB pathway may be therapeutically useful for treating SZ cognitive deficits.

关键词： schizophrenia cognitive impairments cAMP response element binding protein ERK1/2 MK801

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A novel dephosphorylation targeting chimera selectively promoting tau removal in tauopathies

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Signal Transduction and Targeted Therapy 2021年第8期6卷 2511-2520页

作者： Jie Zheng Na Tian Fei Liu Yidian Zhang Jingfen Su Yang Gao Mingmin Deng Linyu Wei Jingwang Ye Honglian Li jian-zhi wang department of pathophysiology School of Basic MedicineKey Laboratory of Education Ministry of China/Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina department of Pharmacology Key Laboratory of Basic Pharmacology of Ministry of EducationJoint International Research Laboratory of Ethnomedicine of Ministry of EducationKey Laboratory of Basic Pharmacology of Guizhou ProvinceZunyi Medical UniversityZunyiChina department of Histology and Embryology Key Laboratory of Ministry of Education for Neurological DisordersSchool of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Co-innovation Center of Neuroregeneration Nantong UniversityNantongChina

Intraneuronal accumulation of hyperphosphorylated tau is a hallmark pathology shown in over twenty neurodegenerative disorders,collectively termed as tauopathies,including the most common Alzheimer's disease(AD).Therefore,selectively removing or reducing hyperphosphorylated tau is promising for therapies of AD and other ***,we designed and synthesized a novel DEPhosphorylation TArgeting Chimera(DEPTAC)to specifically facilitate the binding of tau to Ba-subunit-contalning protein phosphatase 2A(PP2A-Ba),the most active tau phosphatase in the *** DEPTAC exhibited high efficiency in dephosphorylating tau at multiple AD-associated sites and preventing tau accumulation both in vitro and in *** studies revealed that DEPTAC significantly improved microtubule assembly,neurite plasticity,and hippocampus-dependent learning and memory in transgenic mice with inducible overexpression of truncated and neurotoxic human tau *** data provide a strategy for selective removal of the hyperphosphorylated tau,which sheds new light for the targeted therapy of AD and related-tauopathies.

关键词： tau Alzheimer removing

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左旋精氨酸对模拟缺血再灌注乳兔培养窦房结细胞损伤的保护作用(英文)

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实用儿科临床杂志 2008年第13期23卷 1048-1050页

作者：王庆志谭静马全祥高建芝郭义威郭志坤新乡医学院解剖学教研室河南新乡453003 新乡医学院第三附属医院心内科河南新乡453003 新乡医学院病理生理学教研室河南新乡453003

目的观察模拟缺血再灌注(IR)培养乳兔窦房结细胞(SANC)损伤及左旋精氨酸(L-Arg)的保护作用。方法对SANC模拟低糖缺氧培养,添加L-Arg和L-Arg加L-NAME(L-Arg抑制剂)与培养细胞共同孵育,吖啶橙(AO)标记细胞凋亡,检测细胞内过氧化物歧化酶(S... 详细信息

目的观察模拟缺血再灌注(IR)培养乳兔窦房结细胞(SANC)损伤及左旋精氨酸(L-Arg)的保护作用。方法对SANC模拟低糖缺氧培养,添加L-Arg和L-Arg加L-NAME(L-Arg抑制剂)与培养细胞共同孵育,吖啶橙(AO)标记细胞凋亡,检测细胞内过氧化物歧化酶(SOD)活性、丙二醛(MDA)、总一氧化氮合酶(NOS)、氧化亚氮(NO)水平。细胞分为正常对照组、I120R120组、I120R120加L-Arg组、I120R120加L-Arg加L-NAME组4组。结果凋亡细胞体积明显缩小,核呈黄绿色,断裂为多个碎块状,由膜包裹着凸起于细胞表面呈黄绿色凋亡小体。与I120R120组凋亡率[(5.21±1.59)%]比较,I120R120加L-Arg组凋亡率[(8.70±3.10)%]显著降低(P20R120加L-Arg组细胞SOD活性[(46 820±14 450)U/g]较I120R120组[(25 030±8 440)U/g]显著上升,而I120R120加L-Arg组MDA[(5.55±3.71)mmol/g]、NO[(3.65±1.02)U/g]和NOS[(3.73±0.24)μmol/L]较I120R120组MDA[(8.42±4.21)mmol/g]、NO[(4.62±1.20)U/g]和NOS[(4.96±0.52)μmol/L]显著下降(Pa20R120加L-Arg加L-NAME组各指标较I120R120组无显著性差异(Pa>0.05)。结论补充NO合成底物L-Arg能清除自由基,增加SOD活性,增强细胞抗氧化损伤能力,可能是阻断氧自由基所介导的细胞凋亡机制之一。

关键词：缺血-再灌注凋亡 L-精氨酸窦房结细胞培养乳兔

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Mechanisms underlying tau-associated neurodegeneration

Mechanisms underlying tau-associated neurodegeneration

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中国生物化学与分子生物学会2016年全国学术会议

作者： wang jian-zhi department of pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain Science Key Laboratory of Ministry of Education of China for Neurological Disorders Tongji Medical College Huazhong University of Science and Technology

Intracellular accumulation of tau protein,low energy metabolism and mitochondrial dysfunction are core features in the pathophysiology of sporadic Alzheimer’s disease(AD),however,the cellular mechanism whereby tau accumulation links the abnormal energy metabolism is poorly *** found that overexpression of human wild-type full-length tau(termed htau)rendered the cells more resistant to the

关键词： tau neurodegeneration apoptosis mitophagy Alzheimer’s disease

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Magnolol protects against acute gastrointestinal injury in sepsis by down-regulating regulated on activation,normal T-cell expressed and secreted

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World Journal of Clinical Cases 2021年第34期9卷 10451-10463页

作者： Shi-Hao Mao Dan-Dan feng Xi wang Yi-Hui zhi Shu Lei Xi Xing Rong-Lin jiang jian-Nong Wu department of Intensive Care Unit The First Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310006Zhejiang ProvinceChina key laboratory of Digestive pathophysiology of Zhejiang province The First Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310053Zhejiang ProvinceChina

BACKGROUND Sepsis is a major medical *** is an active constituent of Houpu that improves tissue function and exerts strong anti-endotoxin and anti-inflammatory effects,but the mechanism by which it reduces intestinal inflammation in sepsis is yet *** To assess the protective effect of magnolol on intestinal mucosal epithelial cells in sepsis and elucidate the underlying *** Enzyme-linked immunosorbent assay was used to measure tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),IL-6,and regulated on activation,normal T-cell expressed and secreted(RANTES)levels in serum and ileal tissue in animal *** histopathological changes of the ileal mucosa in different groups were observed under a *** Counting Kit-8 and cell permeability assays were used to determine the concentration of drug-containing serum that did not affect the activity of Caco2 cells but inhibited lipopolysaccharide(LPS)-induced decrease in *** and Western blot assays were used to detect the levels of RANTES,inhibitor of nuclear factor kappa-B kinaseβ(IKKβ),phosphorylated IKKβ(p-IKKβ),inhibitor of nuclear factor kappa-B kinaseα(IκBα),p65,and p-p65 proteins in different groups in *** In rats treated with LPS by intravenous tail injection in the presence or absence of magnolol,magnolol inhibited the expression of proinflammatory cytokines,IL-1β,IL-6,and TNF-αin a dose-dependent *** addition,magnolol suppressed the production of RANTES in LPS-stimulated sepsis ***,in vitro studies suggested that magnolol inhibited the increase of p65 nucleation,thereby markedly downregulating the production of the phosphorylated form of IKKβin LPS-treated Caco2 ***,magnolol inhibited the translocation of the transcription factor nuclear factor-kappa B(NF-κB)from the cytosol into the nucleus and down-regulated the expression level of the chemokine RANTES in LPS-stimulated Caco2 *** Magno

关键词： Sepsis Magnolol Regulated on activation,normal T-cell expressed and secreted Anti-inflammation Lipopolysaccharide Nuclear factor-kappa B

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Role and mechanisms underlying tau accumulation-induced neurodegeneration and synapse impairment

Role and mechanisms underlying tau accumulation-induced neur...

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2019全国老年痴呆与认知障碍相关疾病学术大会

作者： wang jian-zhi 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 Technology

As a structural protein,the physiological function of tau proteins is to promote microtubule assembly and maintain the stability of the microtubules,so that to build up the tracks for axonal transport of the *** studies suggest that tau is also actively involved in regulation of cell viability and enzymatic *** Alzheimer disease(AD) and other tauopathies,tau proteins are abnormally hyperphosphorylated or cleaved,or the gene mutated,which result in intracellular tau accumulation and formation of neurofibrillary tangles in the degenerated *** addition to hyperphosphorylation,many other types of tau posttranslational modifications have been identified in the brains of AD patients and/or the transgenic mouse *** date,it is not clear how the abnormality of tau causes neurodegeneration and memory *** overexpressing human full-length wildtype tau to mimic tau abnormality as seen in the brain of sporadic AD patients,we found that tau accumulation activated JAK2 to phosphorylate STAT1 at Tyr701 leading to STAT1 dimerization,nuclear translocation and its ***1 activation suppressed expression of NMDAR through direct binding to the specific GAS element of GluN1,GluN2 A and GluN2 B promoters,while knockdown STAT1 by AAV-Cre in STAT1 flox/flox mice or expressing dominant negative Y701 F-STAT1 efficiently rescued tau-induced suppression of NMDAR expression with amelioration of synaptic functions and memory *** findings indicate that tau accumulation impairs synaptic plasticity through JAK2/STAT1-induced suppression of NMDAR expression,which reveals a novel mechanism for tau-associated synapse and memory deficits in AD and other tauopathies.

关键词： tau accumulation synaptic plasticity NMDA receptors

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Identification of BLA/BLP to hippocampal CA1 circuits

Identification of BLA/BLP to hippocampal CA1 circuits

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中国神经科学学会第十二届全国学术会议

作者： jian-zhi wang department of pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain Science Key Laboratory of Ministry of Education of China for Neurological Disorders Tongji Medical College Huazhong University of Science and Technology

Objective Amygdala is specialized for input and processing of emotions, while the hippocampus is essential for spatial memory. During emotional reactions, these two brain subsets interact to influence spatial cognitive functions. In the coronal sections from rostral to caudal of the brain, the basolateral amygdala is further divided into arterial part（BLA） and posterior part（BLP）. Whether and how BLP interacts with hippocampus remain unclear. The present study is to outline BLP-hippocampus circuit and identify its function. Methods BLP-CA1 circuit was outlined by advanced anterograde and retrograde monosynaptic tracing. Its function was identified by optogenetic manipulation. Results By anterograde and retrograde tracings, we identified a more prominent excitatory neuronal projection from BLP to v CA1, when compared with BLA to v CA1. More importantly, manipulating BLP-v CA1 or BLA-v CA1 circuit differentially affects spatial learning and memory and as well as anxiety behavior. Conclusion BLA-and BLP-v CA1 inputs govern distinct emotion status and differentially influence emotion associated-memory. Further studies will help us understand the brain mechanisms of emotion-regulated cognitive functions and improve clinical treatment of emotionassociated cognitive disorders.

关键词： hippocampus amygdala neural circuit spatial memory anxiety

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Recombinant human erythropoietin ameliorates cognitive dysfunction of APP/PS1 mice by attenuating neuron apoptosis via HSP90β

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Signal Transduction and Targeted Therapy 2022年第6期7卷 1878-1881页

作者： Hua-Li Wan Bing-Ge Zhang Chongyang Chen Qian Liu Ting Li Ye He Yongmei Xie Xifei Yang jian-zhi wang Gong-Ping Liu department of pathophysiology School of Basic MedicineKey Laboratory of Ministry of Education of China and Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina State key laboratory of Biotherapy and Cancer Center West China HospitalSichuan University and Collaborative Innovation Center of BiotherapyChengdu 610041China key laboratory of Modern Toxicology of Shenzhen Shenzhen Medical Key Discipline of Health Toxicology(2020-2024)Shenzhen Center for Disease Control and PreventionShenzhen 518055China Co-innovation Center of Neurodegeneration Nantong UniversityNantongJ.S.China

Dear Editor,Recently,lower hemoglobin/anemia in the elderly is found to be associated with cognitive impairment and Alzheimer’s disease(AD),1 implying that erythropoietin(EPO)may be of benefit for *** a clinically safe-to-use drug,besides its hematopoietic function,recombinant human EPO(rhEPO)is reported to present multifaceted neuroprotective effects.2 Unfortunately,few clinical studies investigated the effect of rhEPO in AD patients.

关键词： protective anemia Alzheimer

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The dual roles of cytokines in Alzheimer’s disease:update on interleukins, TNF-α,TGF-β and IFN-γ

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Translational Neurodegeneration 2016年第1期5卷 52-66页

作者： Cong Zheng Xin-Wen Zhou 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 226000China

Alzheimer’s disease(AD)is one of the most common neurodegenerative disorders in the *** the mechanisms underlying AD neurodegeneration are not fully understood,it is well recognized that inflammation plays a crucial role in the initiation and/or deterioration of AD *** evidence suggests that different cytokines,including interleukins,TNF-α,TGF-βand IFN-γ,are actively participated in AD pathogenesis and may serve as diagnostic or therapeutic targets for AD ***,we review the progress in understanding the important role that these cytokines or neuroinflammation has played in AD etiology and pathogenesis.

关键词： Alzheimer’s disease Cytokines Interleukins TNF-α TGF-β IFN-γ

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Humanin attenuates Alzheimer-like cognitive deficits and pathological changes induced by amyloid β-peptide in rats

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Neuroscience Bulletin 2014年第6期30卷 923-935页

作者： Gao-Shang Chai Dong-Xiao Duan Rong-Hong Ma jian-Ying Shen Hong-Lian Li zhi-Wei Ma Yu Luo Lu wang Xin-Hua Qi Qun wang jian-zhi wang zelan Wei Darrell D.Mousseau Li wang Gongping Liu department of pathophysiology Key Laboratory of Neurological Diseases of Chinese Ministry of EducationTongji Medical CollegeHuazhong University of Science and Technology department of Basic medical Wuxi Medical SchoolJiangnan University department of Physiology Basic Medical CollegeZhengzhou University department of laboratory Medicine Union HospitalHuazhong University of Science and Technology department of Histology and Embryology Tongji Medical CollegeHuazhong University of Science and Technology Affiliated Hospital of Hebei university of Engineering department of Psychiatry College of MedicineUniversity of SaskatchewanSaskatoonSaskatchewanS7N 5E5Canada department of pathophysiology Henan Medical College

Amyloid β-peptide（Aβ） has been implicated as a key molecule in the neurodegenerative cascades of Alzheimer ’s disease（AD）. Humanin（HN） is a secretory peptide that inhibits the neurotoxicity of Aβ. However, the mechanism（s） by which HN exerts its neuroprotection against Aβ-induced ADlike pathological changes and memory deficits are yet to be completely defined. In the present study,we provided evidence that treatment of rats with HN increases the number of dendritic branches and the density of dendritic spines, and upregulates pre- and post-synaptic protein levels; these effects lead to enhanced long-term potentiation and amelioration of the memory deficits induced by Aβ1-42. HN also attenuated Aβ1-42-induced tau hyperphosphorylation,apparently by inhibiting the phosphorylation of Tyr307 on the inhibitory protein phosphatase-2A（PP2A）catalytic subunit and thereby activating PP2 A. HN also inhibited apoptosis and reduced the oxidativestress induced by Aβ1-42. These findings provide novel mechanisms of action for the ability of HN to protect against Aβ1-42-induced AD-like pathological changes and memory deficits.

关键词： Humanin amyloid-beta Alzheimer’s disease tau apoptosis

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