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Lack of interferon regulatory factor 3 leads to anxiety/depression-like behaviors through disrupting the balance of neuronal excitation and inhibition in mice

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Genes & Diseases 2023年第3期10卷 1062-1074页

作者： Junjie Li Yayan Pang Yehong Du Lei Xia Mulan Chen Yepeng Fan Zhifang Dong Pediatric Research Institute Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory DisordersChildren's Hospital of Chongqing Medical UniversityChongqing 400014China

Disrupting the balance of neuronal excitation and inhibition (E/I) is an important pathogenic mechanism of anxiety and depression. Interferon regulatory factor 3 (IRF3) plays a key role in the innate immune response, and activation of IRF3 triggers the expression of type I interferons and downstream interferon-stimulated genes, which are associated with anxiety and depression. However, whether IRF3 participates in the pathogenesis of anxiety/depression by regulating E/I balance remains poorly understood. Here, we reported that global knockout (KO) of IRF3 (IRF3^(−/−)) significantly increased anxiety/depression-like behaviors, but did not affect normal spatial learning and memory. Compared with wild type (WT) control mice, the E/I balance was disrupted, as reflected by enhanced glutamatergic transmission and decreased GABAergic transmission in the neurons of hippocampal CA1 and medial prefrontal cortex (mPFC) in IRF3-KO mice. Importantly, genetic rescue of IRF3 expression by adeno-associated virus (AAV) was sufficient to alleviate anxiety/depression-like behaviors and restore the neuronal E/I balance in IRF3-KO mice. Taken together, our results indicate that IRF3 is critical in maintaining neuronal E/I balance, thereby playing an essential role in ensuring emotional stability.

关键词： Anxiety Depression Hippocampus IRF3 Medial prefr ontal cortex Synaptic transmission

An effective strategy for dendrite free Li metal anodes:Nickel foam decorated with high lattice-matching CoN and CoF_(2) nanosheets for dense deposition

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Nano Research 2024年第5期17卷 4069-4078页

作者： Wenlong Liu Jianzong Man Xiaodong Sun Ning Zhang Yehong Du Kun Liu Zhongsheng Wen Song Li Juncai Sun Institute of Materials and Technology Dalian Maritime UniversityDalian 116026China Shandong Provinvial Key Laboratory of Chemical Energy Storage and Novel Cell Technology and School of Chemistry and Chemical enginneringLiaocheng UniversityLiaocheng 252000China Department of Public Security Management Liaoning Police CollegeDalian 116036China

The notorious dendrite and infinite volume change seriously restrict the advancement of lithium metal anodes(LMAs),during the long-term process of stripping/plating.Herein,the nanosheets of metal fluoride(CoF_(2))and metal nitride(CoN)with magnificent lithiophilicity on the nickel(Ni)foam are designed as the“regulator”to uniform the Li plating and build stronger solid electrolyte interface(SEI)layer for dendrite free LMAs.The Ni foam offers abundant space to receive deposited Li metal.The CoN nanosheets can guarantee the fast transfer of electrons,which provides a stable interface of Li^(+)reduction.Moreover,the nanosheet structure with lithiophilicity would accelerate the move of Li+and decrease the nucleation barrier,due to the high lattice-matching of Li and CoN.Meanwhile,the CoF_(2) could increase the content of F(LiF)in the SEI layer,which enhances the strength and avoids the destruction of SEI layer.With the cooperation of CoN and CoF_(2),the composited anode(Li/NF@CNCF)exhibits ultra-long cycle performance(more than 1200 h)and fantastic structure stability at 1 mA·cm^(-2) with 1 mAh·cm^(-2).Based on the LiFePO_(4) and Li/NF@CNCF,the full cells deliver excellent specifical capacity and steady coulombic efficiency.The strategy contributes an effective approach to alleviate the issues of lithium metal anodes in the field of LMAs.

关键词： CoN and CoF_(2) lattice-matching nanosheet lithiophilicity lithium metal anodes

MKP-1 reduces Aβ generation and alleviates cognitive impairments in Alzheimer’s disease models

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Signal Transduction and Targeted Therapy 2019年第1期4卷 149-160页

作者： Yehong Du Yexiang du Yun Zhang Zhilin Huang Min Fu Junjie Li Yayan Pang Peng Lei Yu Tian Wang Weihong Song Guiqiong He Zhifang Dong Pediatric Research Institute Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory DisordersChildren’s Hospital of Chongqing Medical UniversityChongqing400014PR China Department of Anatomy Basic Medical CollegeChongqing Medical UniversityChongqing400016PR China Townsend Family Laboratories Department of PsychiatryThe University of British ColumbiaVancouverBCV6T 1Z3Canada West China School of Basic Medical Sciences and Forensic Medicine Sichuan UniversityChengdu610041SichuanChina Brain Research Centre The University of British ColumbiaVancouverBCV6T 2B5Canada

Mitogen-activated protein kinase(MAPK)phosphatase 1(MKP-1)is an essential negative regulator of MAPKs by dephosphorylating MAPKs at both tyrosine and threonine residues.Dysregulation of the MAPK signaling pathway has been associated with Alzheimer’s disease(AD).However,the role of MKP-1 in AD pathogenesis remains elusive.Here,we report that MKP-1 levels were decreased in the brain tissues of patients with AD and an AD mouse model.The reduction in MKP-1 gene expression appeared to be a result of transcriptional inhibition via transcription factor specificity protein 1(Sp1)cis-acting binding elements in the MKP-1 gene promoter.Amyloid-β(Aβ)-induced Sp1 activation decreased MKP-1 expression.However,upregulation of MKP-1 inhibited the expression of both Aβprecursor protein(APP)andβ-site APP-cleaving enzyme 1 by inactivating the extracellular signal-regulated kinase 1/2(ERK)/MAPK signaling pathway.Furthermore,upregulation of MKP-1 reduced Aβproduction and plaque formation and improved hippocampal long-term potentiation(LTP)and cognitive deficits in APP/PS1 transgenic mice.Our results demonstrate that MKP-1 impairment facilitates the pathogenesis of AD,whereas upregulation of MKP-1 plays a neuroprotective role to reduce Alzheimer-related phenotypes.Thus,this study suggests that MKP-1 is a novel molecule for AD treatment.

关键词： Alzheimer Aβ impairment

miR-429-3p mediates memory decline by targeting MKP-1 to reduce surface GluA1- containing AMPA receptors in a mouse model of Alzheimer’s disease

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Acta Pharmaceutica Sinica B 2024年第2期14卷 635-652页

作者： Man Luo Yayan Pang Junjie Li Lilin Yi Bin Wu Qiuyun Tian Yan He Maoju Wang Lei Xia Guiqiong He Weihong Song Yehong Du Zhifang Dong Pediatric Research Institute Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory DisordersChildren’s Hospital of Chongqing Medical UniversityChongqing 400014China Department of Anatomy Basic Medical CollegeChongqing Medical UniversityChongqing 400016China Townsend Family Laboratories Department of PsychiatryThe University of British ColumbiaVancouver BC V6T 1Z3Canada Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)Institute of AgingKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceZhejiang Clinical Research Center for Mental DisordersSchool of Mental Health and the Affiliated Kangning HospitalWenzhou Medical UniversityWenzhou 325000China Institute for Brain Science and Disease of Chongqing Medical University Chongqing 400016China

Alzheimer ’s disease(AD) is a leading cause of dementia in the elderly.Mitogen-activated protein kinase phosphatase 1(MKP-1) plays a neuroprotective role in AD.However,the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied.MicroRNAs(miRNAs) regulate gene expression at the post-transcriptional level,thereby repressing mRNA translation.Here,we reported that the microRNA-429-3p(miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2AAPPAD model cells.We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3’-untranslated region(3’ UTR).Inhibition of miR-429-3p by its antagomir(A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation.More importantly,intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase(ERK1/2)-mediated GluAl hyperphosphorylation at Ser831 site,thereby increasing the surface expression of GluAl-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors(AMPARs).Together,these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice,suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment.

关键词： Alzheimer's disease MKP-1 miR-429-3p AMPAreceptor Learning and memory Long-term potentiation

Glutamate and GABAA receptor crosstalk mediates homeostatic regulation of neuronal excitation in the mammalian brain

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Signal Transduction and Targeted Therapy 2022年第11期7卷 4156-4173页

作者： Ya Wen Zhifang Dong Jun Liu Peter Axerio-Cilies Yehong Du Junjie Li Long Chen Lu Zhang Lidong Liu Jie Lu Ning Zhou Dong Chuan Wu Yu Tian Wang DM Centre for Brain Health and Department of Medicine Vancouver Coastal Health Research InstituteUniversity of British ColumbiaVancouverBCV6T 2B5Canada Pediatric Research Institute Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory DisordersChildren’s Hospital of Chongqing Medical UniversityChongqing400014P.R.China iHuman Institue ShanghaiTech UniversityShanghaiP.R.China

Maintaining a proper balance between the glutamate receptor-mediated neuronal excitation and the A type of GABA receptor(GABAAR)mediated inhibition is essential for brain functioning;and its imbalance contributes to the pathogenesis of many brain disorders including neurodegenerative diseases and mental illnesses.Here we identify a novel glutamate-GABAAR interaction mediated by a direct glutamate binding of the GABAAR.In HEK293 cells overexpressing recombinant GABAARs,glutamate and its analog ligands,while producing no current on their own,potentiate GABA-evoked currents.This potentiation is mediated by a direct binding at a novel glutamate binding pocket located at theα+/β−subunit interface of the GABAAR.Moreover,the potentiation does not require the presence of aγsubunit,and in fact,the presence ofγsubunit significantly reduces the potency of the glutamate potentiation.In addition,the glutamate-mediated allosteric potentiation occurs on native GABAARs in rat neurons maintained in culture,as evidenced by the potentiation of GABAAR-mediated inhibitory postsynaptic currents and tonic currents.Most importantly,we found that genetic impairment of this glutamate potentiation in knock-in mice resulted in phenotypes of increased neuronal excitability,including decreased thresholds to noxious stimuli and increased seizure susceptibility.These results demonstrate a novel cross-talk between excitatory transmitter glutamate and inhibitory GABAAR.Such a rapid and short feedback loop between the two principal excitatory and inhibitory neurotransmission systems may play a critical homeostatic role in fine-tuning the excitation-inhibition balance(E/I balance),thereby maintaining neuronal excitability in the mammalian brain under both physiological and pathological conditions.

关键词： excitation thereby maintained

Discovery of a normal-tension glaucoma-suspect rhesus macaque with craniocerebral injury:Hints of elevated translaminar cribrosa pressure difference

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Chinese Medical Journal 2024年第4期137卷 484-486页

作者： Jian Wu Qi Zhang Xu Jia Yingting Zhu Zhidong Li Shu Tu Ling Zhao Yifan du Wei Liu Jiaoyan Ren Liangzhi Xu Hanxiang Yu Fagao Luo Wenru Su Ningli Wang yehong Zhuo State Key Laboratory of Ophthalmology Zhongshan Ophthalmic CenterGuangdong Provincial Key Laboratory of Ophthalmology and Visual ScienceSun Yat-sen UniversityGuangzhouGuangdong 510060China Beijing Institute of Ophthalmology Beijing Tongren Eye CenterBeijing Tongren HospitalCapital Medical UniversityBeijing Ophthalmology&Visual Sciences Key LaboratoryBeijing 100730China School of Food Sciences and Engineering South China University of TechnologyGuangzhouGuangdong 510641China Guangzhou Huazhen Biosciences GuangzhouGuangdong 510920China

To the Editor:Normal-tension glaucoma(NTG)is a progressive optic neuropathy characterized by irreversible blindness with statistically normal intraocular pressure(IOP)(≤21 mmHg),^([1,2])which makes early-stage diagnosis in the clinical practice difficult.Pathophysiological pathways underlying NTG include vascular dysregulation,toxic metabolite accumulation,and elevated translaminar cribrosa pressure difference(TLCPD).^([3])Although various small animal models have provided evidence of different pathophysiological mechanisms,the complicated clinical phenotype cannot be fully imitated by secondary disease models,and the gap between rodents and humans weakens their translational potential.Thus,the pathological changes associated with NTG remain unclear.

关键词： elevated glaucoma diagnosis

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论新媒体时代我国新闻工作者职业道德建设

理论界 2014年第10期 60-63页

作者：都业虹半岛晨报社辽宁大连116013

新媒体时代以其鲜明的特征,对新闻道德产生强烈冲击,有的新闻工作者表现出宗旨淡漠,逐利增强,真实性下降,引导性乏力等职业道德失范现象。新闻工作者需要加强职业道德建设,明确为人民服务的宗旨,提升思想境界,胸怀大局、把握大势、着眼... 详细信息

新媒体时代以其鲜明的特征,对新闻道德产生强烈冲击,有的新闻工作者表现出宗旨淡漠,逐利增强,真实性下降,引导性乏力等职业道德失范现象。新闻工作者需要加强职业道德建设,明确为人民服务的宗旨,提升思想境界,胸怀大局、把握大势、着眼大事,加强马克思主义新闻观的学习,追求报道的真实性,坚守新闻工作的道德底线,承担起时代所赋予的历史责任,为推动传统媒体和新兴媒体融合发展发力,为全面建设小康社会贡献力量。

关键词：新媒体新闻工作者职业道德

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煤巷顶板分布式光纤监测的可行性试验研究

矿业安全与环保 2022年第5期49卷 81-88页

作者：杜传伟胡涛李业宏王嘉钰齐鲁理工学院土木工程学院山东济南250200 山东省煤炭技术服务有限责任公司山东济南250032

在传统顶板点式监测的基础上,应用BOTDR对采煤工作面回采巷道煤巷顶板沉降位移进行分布式监测。首先通过对BOTDR监测原理和煤巷顶板变形状态的理论分析,提出应用锚杆(索)在煤巷顶板进行光纤定点布设,并根据BOTDR测量的相邻定点间光纤轴... 详细信息

在传统顶板点式监测的基础上,应用BOTDR对采煤工作面回采巷道煤巷顶板沉降位移进行分布式监测。首先通过对BOTDR监测原理和煤巷顶板变形状态的理论分析,提出应用锚杆(索)在煤巷顶板进行光纤定点布设,并根据BOTDR测量的相邻定点间光纤轴向应变和变形量,推导出光纤应变量化煤巷顶板沉降位移的数学表达式;然后进行煤巷顶板沉降的光纤定点拉伸和区段拉伸室内模拟试验,试验中光纤应变表征的位移与光纤拉伸距离的误差分别为0.690%和1.545%,拉伸距离和应变表征光纤位移基本一致;最后进行了采煤工作面回采过程中进风巷煤巷顶板的BOTDR现场监测试验,试验期间,光纤应变表征出最大沉降位移平均值为64.09 mm和135.63 mm的2个顶板沉降区域。与井下十字观测法测量值相比,顶板沉降变形范围的最大误差为5.60%,顶板沉降位移的最大误差为4.96%,顶板垂直位移的绝对误差值小于4 mm,证明了BOTDR定量表征顶板的沉降变形范围和沉降位移的可行性。

关键词：煤巷顶板沉降位移分布式光纤监测布里渊时域反射技术

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肉苁蓉和管花肉苁蓉种子萌发及质量研究

种子 2023年第4期42卷 108-117页

作者：朱文娟郭晔红姜侃杜弢陈垣甘肃农业大学农学院/省部共建干旱生境作物学国家重点实验室兰州730070 甘肃中医药大学兰州730000

以肉苁蓉种子和管花肉苁蓉种子为研究对象,采用赤霉素、氟啶酮、氟草敏处理种子,探索两种肉苁蓉种子快速萌发的条件,并制订肉苁蓉和管花肉苁蓉种子质量检验规程。结果表明,以赤霉素预处理种子后,经氟啶酮或氟草敏培养,可显著提高种子的... 详细信息

以肉苁蓉种子和管花肉苁蓉种子为研究对象,采用赤霉素、氟啶酮、氟草敏处理种子,探索两种肉苁蓉种子快速萌发的条件,并制订肉苁蓉和管花肉苁蓉种子质量检验规程。结果表明,以赤霉素预处理种子后,经氟啶酮或氟草敏培养,可显著提高种子的发芽率和发芽势。肉苁蓉种子的最佳萌发条件为25℃黑暗下,种子在蒸馏水中吸胀24 h,以1 000 mg/L赤霉素预处理72 h, 0.01 mg/L氟啶酮培养21 d;管花肉苁蓉种子的最佳萌发条件为25℃黑暗下,种子在蒸馏水中吸胀24 h,以1 mg/L赤霉素预处理72 h, 100 mg/L氟啶酮培养21 d。

关键词：肉苁蓉管花肉苁蓉种子萌发种子质量检验