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Hearing impairment-associated KARS mutations lead to defects in aminoacylation of both cytoplasmic and mitochondrial tRNA^(Lys)

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Science China(Life Sciences) 2020年第8期63卷 1227-1239页

作者： Yong Wang Jing-Bo Zhou qi-yu zeng Siqi Wu Mei-qin Xue Pengfei Fang En-Duo Wang Xiao-Long Zhou State Key Laboratory of Molecular Biology CAS Center for Excellence in Molecular Cell ScienceShanghai Institute of Biochemistry and Cell BiologyChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China State Key Laboratory of Bioorganic and Natural Products Chemistry Center for Excellence in Molecular SynthesisShanghai Institute of Organic ChemistryChinese Academy of SciencesShanghai 200032China

Aminoacyl-tRNA synthetases(aaRSs)are ubiquitously expressed,essential enzymes,synthesizing aminoacyl-tRNAs for protein *** defects of aaRSs frequently cause various human *** KARS encodes both cytosolic and mitochondrial lysyl-tRNA synthetases(LysRSs).Previously,two mutations(c.1129 G>A and c.517 T>C)were identified that led to hearing impairment;however,the underlying biochemical mechanism is *** the present study,we found that the two mutations have no impact on the incorporation of LysRS into the multiple-synthetase complex in the cytosol,but affect the cytosolic LysRS level,its tertiary structure,and cytosolic tRNA aminoacylation in *** for mitochondrial translation,the two mutations have little effect on the steady-state level,mitochondrial targeting,and tRNA binding affinity of mitochondrial ***,they exhibit striking differences in charging mitochondrial tRNALys,with the c.517T>C mutant being completely deficient in vitro and in *** constructed two yeast genetic models,which are powerful tools to test the in vivo aminoacylation activity of KARS mutations at both the cytosolic and mitochondrial ***,our data provided biochemical insights into the potentially molecular pathological mechanism of KARS c.1129G>A and c.517T>C mutations and provided yeast genetic bases to investigate other KARS mutations in the future.

关键词： aminoacyl-tRNA synthetase tRNA aminoacylation protein synthesis

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Endoplasmic Reticulum Stress Induces the Early Appearance of Pro-apoptotic and Anti-apoptotic Proteins in Neurons of Five Familial Alzheimer＇s Disease Mice

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Chinese Medical Journal 2016年第23期129卷 2845-2852页

作者： Hui Shen Xiao-Dong Pan Jing Zhang yu-qi zeng Meng Zhou Lu-Meng Yang Bing Ye Xiao-Man Dai yuan-Gui Zhu Xiao-Chun Chen Department of Neurology and Geriatrics Fujian Institute of Geriatrics Fujian Medical University Union Hospital Fuzhou Fujian 350001 China Key Laboratory of Brain Aging and Neurodegenerative Diseases Fujian Key Laboratory of Molecular Neurology Fujian Medical University Fuzhou Fujian 350001 China

Background： Amyloid β （Aβ） deposits and the endoplasmic reticulum stress （ERS） are both well established in the development and progression of Alzheimer＇s disease （AD）. However, the mechanism and role of Aβ-induced ERS in AD-associated pathological progression remain to be elucidated. Methods： The five familial AD （5×FAD） mice and wild-type （WT） mice aged 2, 7, and 12 months were used in the present study. Monis water maze test was used to evaluate their cognitive performance, lmmunofluorescence and Western blot analyses were used to examine the dynamic changes of pro-apoptotic （CCAAT/enhancer-binding protein homologous protein [CHOP] and cleaved caspase-12） and anti-apoptotic factors （chaperone glucose-regulated protein [GRP] 78 and endoplasmic reticulum-associated protein degradation-associated ubiquitin ligase synovial apoptosis inhibitor 1 [SYVN 1]） in the ERS-associated unfolded protein response （UPR） pathway. Results： Compared with age-matched WT mice, 5 xFAD mice showed higher cleaved caspase-3, lower neuron-positive staining at the age of 12 months, but earlier cognitive deficit at the age of 7 months （all P 〈 0.05）. Interestingly, for 2-month-old 5×FAD mice, the related proteins involved in the ERS-associated UPR pathway, including CHOP, cleaved caspase-12, GRP 78, and SYVN 1, were significantly increased when compared with those in age-matched WT mice （all P 〈 0.05）. Moreover, ERS occurred mainly in neurons, not in astrocytes. Conclusions： These findings suggest that compared with those of age-matched WT mice, ERS-associated pro-apoptotic and anti-apoptotic proteins are upregulated in 2-month-old 5×FAD mice, consistent with intracellular Aβ aggregation in neurons.

关键词： Alzheimer's Disease Amyloid β Apoptosis: Endoplasmic Reticulum Stress Unfolded Protein Response Pathway

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Curcumin protects mitochondria from oxidative damage and attenuates apoptosis in cortical neurons

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Acta Pharmacologica Sinica 2004年第12期25卷 40-46页

作者： yuan-gui ZHU2, Xiao-chun CHEN3, Zhi-zhe CHEN4, yu-qi zeng, Guang-bin SHI, Yan-hua SU, Xu PENG Fujian Instituteof Geriatrics, Fujian Institute of Hematology, Union Hospital, Fujian Medical University, Fuzhou 350001, China 2Now in Rush University Medical Center, Chicago, IL 60612,USA. Fujian Institute of Geriatrics Fujian Institute of Hematology Union Hospital Fujian Medical University Fuzhou 350001 Chin

AIM: To investigate the effect of curcumin on tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in rat cortical neurons and to explore the possible mechanism. METHODS: Primary cultured rat cortical neurons were performed in vitro and cell viability was measured by MTT assay. DNA fragmentation was used to evaluate cell apoptosis. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (?Ψm) was deter- mined by flow cytometric assay. Cellular glutathione (GSH) content was measured by spectrophotometer. Bcl-2 family proteins, cytochrome c, cleaved caspase-3, and poly (ADP-ribose) polymerase (PARP) were detected by Western blot. RESULTS: Exposure of tBHP 100 μmol/L to neurons for 60 min resulted in ?Ψm loss and cyto- chrome c release from mitochondria and subsequent activationof caspase-3 and PARP cleavation, and cell apoptosis. After removal of tBHP and then further treatment with curcumin (2.5-20 μmol/L) for 18 h, curcumin abrogated ?Ψm loss and cytochrome c release, blocked activation of caspase3, and altered the expression of Bcl-2 family. Further curcumin treatment also prevented cellular GSH and decreased intracellular ROS generation markedly. Curcumin eventually attenuated tBHP-induced apoptosis in cortical neurons. CONCLUSION: Curcumin may attenuate oxidative damages in cortical neurons by reducing intracellular production of ROS and protecting mito- chondria from oxidative damage.

关键词： Curcumin tert-butyl hydroperoxide apoptosis oxidative stress Bcl-2 family proteins mitochondria Alzheimerdisease

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血小板源性生长因子-D和表皮生长因子受体Ⅲ型突变体在膀胱移行细胞癌中的表达及其临床意义

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中国生物制品学杂志 2012年第9期25卷 1203-1206,1210页

作者：杨平苟欣陈雪莲齐玉增重庆医科大学第一附属医院泌尿外科重庆400016 四川省遂宁市第一人民医院妇产科四川遂宁629000

目的探讨血小板源性生长因子-D(Platelet-derived growth factor D,PDGF-D)和表皮生长因子受体Ⅲ型突变体(Epidermal growth factor receptor typeⅢmutant,EGFRvⅢ)在膀胱移行细胞癌(Bladder transitional cell carcinoma,BTCC)中的表达及其临床意义。方法分别采用RT-PCR法和免疫组织化学SP法检测PDGF-D和EGFRvⅢ在80例BTCC组织和10份癌旁正常组织中的转录及表达情况,并分析二者与患者临床病理特征之间的相关性。结果 BTCC组织中PDGF-D和EGFRvⅢ在mRNA和蛋白水平上的表达均显著高于癌旁正常组织(P0.05);PDGF-D与EGFRvⅢ的表达呈正相关(r=0.994,P<0.01)。结论 PDGF-D和EGFRvⅢ在BTCC组织中的表达与病理分级及TNM分期明显相关,可作为判断BTCC恶性程度、浸润与进展的重要生物学指标。

关键词：膀胱移行细胞癌血小板源性生长因子表皮生长因子受体

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Visible-light-responsive homologous heterostructure of oxynitrides constructed to boost charge separation and water splitting

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Science China Chemistry 2025年第01期 186-191页

作者： Hai Zou yunfeng Bao Xueshang Xin yu qi Tengfeng Xie Fuxiang Zhang State Key Laboratory of Catalysis Dalian National Laboratory for Clean Energy Dalian Institute of Chemical Physics Chinese Academy of Sciences School of Chemistry and Chemical Engineering Liaoning Normal University College of Chemistry Jilin University

Constructing type II heterostructures represents a widely recognized strategy for enhancing charge separation and photocatalytic efficiency,but it remains challenging to fabricate homologous heterostructures based on visible-light-responsive semiconductors,especially for popularly investigated （oxy）nitrides with low thermal ***,we synthesized a homologous heterostructure （denoted as YTON＿H） based on the oxynitrides of YTaO4-xNyand YTa *** heterostructure exhibits type II band structure alignment and intimate interface achieved through a magnesium （Mg） powder-assisted nitridation *** with widely reported heterologous heterostructures,the as-obtained YTON＿H homologous heterostructure could similarly exhibit enhanced charge separation as well as photocatalytic water splitting performance with respect to its counterparts(YTaO4-xNyand YTaON2).Meanwhile,detailed structural characterizations and spectroscopy analysis have been made to confirm the formation of heterostructure and promotion of spatial charge separation.

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Multilevel analysis of the central-peripheral-target organ pathway:contributing to recovery after peripheral nerve injury

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Neural Regeneration Research 2025年第10期20卷 2807-2822页

作者： Xizi Song Ruixin Li Xiaolei Chu qi Li Ruihua Li qingwen Li Kai-yu Tong Xiaosong Gu Dong Ming Academy of Medical Engineering and Translational Medicine Tianjin UniversityTianjinChina Haihe Laboratory of Brain-Machine Interface and Human-Machine Fusion TianjinChina Department of Rehabilitation Tianjin University Tianjin HospitalTianjinChina Department of Hand Microsurgery Tianjin University Tianjin HospitalTianjinChina School of Exercise and Health Tianjin University of SportTianjinChina Department of Biomedical Engineering the Chinese University of Hong KongHong Kong Special Administrative RegionChina

Peripheral nerve injury is a common neurological condition that often leads to severe functional limitations and *** on the pathogenesis of peripheral nerve injury has focused on pathological changes at individual injury sites,neglecting multilevel pathological analysis of the overall nervous system and target *** has led to restrictions on current therapeutic *** this paper,we first summarize the potential mechanisms of peripheral nerve injury from a holistic perspective,covering the central nervous system,peripheral nervous system,and target *** peripheral nerve injury,the cortical plasticity of the brain is altered due to damage to and regeneration of peripheral nerves;changes such as neuronal apoptosis and axonal demyelination occur in the spinal *** nerve will undergo axonal regeneration,activation of Schwann cells,inflammatory response,and vascular system regeneration at the injury *** damage to target organs can occur,including skeletal muscle atrophy and sensory receptor *** then provide a brief review of the research advances in therapeutic approaches to peripheral nerve *** main current treatments are conducted passively and include physical factor rehabilitation,pharmacological treatments,cell-based therapies,and physical ***,most treatments only partially address the problem and cannot complete the systematic recovery of the entire central nervous system-peripheral nervous system-target organ ***,we should further explore multilevel treatment options that produce effective,long-lasting results,perhaps requiring a combination of passive(traditional)and active(novel)treatment methods to stimulate rehabilitation at the central-peripheral-target organ levels to achieve better functional recovery.

关键词： central nervous system central peripheral target organ multilevel pathological analysis nerve regeneration peripheral nerve injury peripheral nervous system target organs therapeutic approach

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在共培养体系中单克隆抗体AH_6对小鼠胚泡着床的影响

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动物学报 1998年第4期44卷 443-449页

作者：王晓琦曹宇静曾国庆朱正美中国科学院动物研究所计划生育生殖生物学国家重点实验室大连医科大学生化教研室生殖生化研究室

以单克隆抗体ＡＨ６［特异结合ＬｅＹ寡糖，Ｆｕｃα１２Ｇａｌβ１４（Ｆｕｃα１３）ＧｌｃＮＡｃ］以及其它３种与ＬｅＹ寡糖结构近似的寡糖特异结合的单克隆抗体αＬｅａ、αＬｅｂ和ＦＥＡ５为工具，采用小鼠体外着床模... 详细信息

以单克隆抗体ＡＨ６［特异结合ＬｅＹ寡糖，Ｆｕｃα１２Ｇａｌβ１４（Ｆｕｃα１３）ＧｌｃＮＡｃ］以及其它３种与ＬｅＹ寡糖结构近似的寡糖特异结合的单克隆抗体αＬｅａ、αＬｅｂ和ＦＥＡ５为工具，采用小鼠体外着床模型，研究细胞表面ＬｅＹ寡糖抗原与着床的关系及其在着床过程中的具体作用环节。结果显示：不论子宫上皮细胞表面还是胚胎滋养层细胞表面的ＬｅＹ寡糖抗原被封闭后，都能导致胚胎在单层子宫上皮细胞表面粘附和扩展生长的延迟，但对胚胎最终的扩展程度并无影响，而其它３种单克隆抗体对胚胎的粘附则均无影响。说明这种作用具有明确的寡糖结构特异性。另外，运用免疫荧光方法观察到，胚胎在单层子宫上皮细胞表面的粘附与ＬｅＹ寡糖在细胞表面的消长密切相关。因而认为ＬｅＹ寡糖抗原在胚胎着床中可能是作为一种中介分子参与着床始发阶段的胚胎与母体间的识别和粘着。实验中经单克隆抗体处理后胚胎和单层子宫上皮细胞与对照组比较，其形态与发育未见不同。

关键词：单克隆抗体AH6 Le^Y寡糖抗原小鼠体外着床

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骨髓间充质干细胞移植在小鼠急性肾损伤肾内的存活与分化情况研究

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生命科学研究 2011年第6期15卷 471-475页

作者：齐玉增苟欣周青松杨平重庆医科大学附属第一医院泌尿外科中国重庆400016

为探讨急性肾损伤后,移植骨髓间充质干细胞(marrow mesenchymal stem cells,MSCs)在损伤肾内的存活能力及分化情况,通过复苏、扩增培养已完成鉴定、经慢病毒EGFP转染的MSCs,观察备用MSCs的EGFP(enhanced green fluorescent protein)表... 详细信息

为探讨急性肾损伤后,移植骨髓间充质干细胞(marrow mesenchymal stem cells,MSCs)在损伤肾内的存活能力及分化情况,通过复苏、扩增培养已完成鉴定、经慢病毒EGFP转染的MSCs,观察备用MSCs的EGFP(enhanced green fluorescent protein)表达情况,采用雄性C57BL/6J小鼠12只建立小鼠肾脏缺血再灌注损伤模型后(结扎双侧肾蒂40 min后开放血流并经尾静脉注射MSCs),分别于第1、3、7、14 d处死3只小鼠,采集小鼠左侧肾脏制作石蜡切片,倒置荧光显微镜下观察MSCs在肾内的存活及分化情况,定量分析每个时间点存活于肾内的数目的差异.结果表明复苏、扩增培养出的MSCs增殖活力旺盛,成功建立小鼠肾脏缺血再灌注损伤模型.移植的细胞随时间的延长,存活于肾脏内的数量显著减少(第14 d存活于肾内的细胞数量仅为移植后第1d的1/5),第1、3、7、14 d表达EGFP的MSCs主要分布于肾小球周围、肾脏小血管内壁、肾小管与肾小管之间的间质而肾小管内壁未见到表达EGFP的MSCs分布.这说明移植的MSCs在缺血再灌注损伤后肾脏内能够存活,但肾脏内的微环境限制了移植细胞的存活能力.在肾小管内壁未观测到表达EGFP的MSCs,提示MSCs对肾脏修复的途径不是直接向肾小管内皮细胞分化而另有其它途径.

关键词：骨髓间充质干细胞(MSCs) 缺血再灌注存活分化

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Synergistic removal of nitrogen monoxide by non-thermal plasma and catalyst simultaneously

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Journal of Environmental Sciences 2005年第5期17卷 846-848页

作者： yu Gang yu qi zeng Ke-si ZHAI Xiao-dong Department of Man-Machine and Environment Engineering College of Aerospace Engineering Nanjing University of Aeronautics and AstronauticsNanjing 210016 China College of Environmental and Chemical Engineering Wuhan Institute of Science and Technology Wuhan 430074 China

An experimental system of De-NO with plasma-catalyst（Cu zeolite） was established to investigate the differences between De- NO with plasma-catalyst and De-NO only with plasma, to provide the instruction for selecting appropriate catalyst and operating condition, The characteristics of De-NO with plasma and De-NO with plasma-catalyst were investigated comparatively by experiments. The experimental results show that De-NO with plasma-catalyst has high NO removal rate; Cu zeolite is an effective catalyst which can promote NO removal rate in plasma remarkably; De-NO with plasma-catalyst should be operated at low temperature and the temperature has opposite effects on the function of catalvst and plasma; water vapor and O2 can increase the NO removal rate.

关键词： nitrogen monoxide( NO) synergistic removal non-thermal plasma catalyst De-NO

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去亚甲基小檗碱的药理作用研究进展

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中国药理学通报 2025年第1期41卷 7-12页

作者：李靖琪张琪陈雨桐仝永斌鲁澄宇广东医科大学药学院广东东莞523808

去亚甲基小檗碱(demethyleneberberine,DMB)是小檗碱在体内的主要代谢产物之一,其具有广泛的药理特性。大量研究表明其具有改善感染、抗炎、抗纤维化、抑制癌细胞、调节血脂等多种生物活性,而且在神经退行性疾病治疗领域有巨大潜力。该... 详细信息

去亚甲基小檗碱(demethyleneberberine,DMB)是小檗碱在体内的主要代谢产物之一,其具有广泛的药理特性。大量研究表明其具有改善感染、抗炎、抗纤维化、抑制癌细胞、调节血脂等多种生物活性,而且在神经退行性疾病治疗领域有巨大潜力。该文通过对DMB药理作用及其机制进行系统概述,以期为深入理解其药理作用及合理开发提供科学依据。

关键词：去亚甲基小檗碱药理作用抗感染抗炎肝保护神经保护

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