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Thermal preconditioning protected cerebellar granule neurons of rats by modulating HSP70 expression

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Acta Pharmacologica Sinica 2004年第4期25卷 60-63页

作者： Li-jun CHEN, Xing-wen SU, Peng-xin QIU, Yi-junHUANG, Guang-mei YAN2 Department of Pharmacology, Zhongshan MedicalCollege, Sun Yat-Sen University, Guangzhou 510089, China Department of Pharmacology Zhongshan Medical College Sun Yat-Sen University

AIM: To explore the possibility that expressions of different heat shock proteins (HSPs) are specifically involved in the protection of thermal preconditioning against apoptosis of cerebellar granule neurons (CGNs) induced by repolarization. METHODS: Western blotting was used to detect expressions of HSP27, HSP70, and HSP90 in- duced by thermal preconditioning (TP) in CGNs; reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression level of HSP70 mRNA; apoptosis of CGNs was induced by switching culture medium containing KCl 25 mmol/L to one containing KCl 5 mmol/L. RESULTS: No expression of HSP27 in cerebellar granule neurons was observed with TP at 44 oC. Expression of HSP90 was obvious in CGNs both without and with TP at 44 oC for different periods. Expression of HSP70 protein in CGNs was lower with TP at 44 oC for 5 min, but it increased gradually after the period was prolonged to 30, 60, or 90 min. HSP70 mRNA was detected after TP 44 oC for 30, 60, and 90 min and increased gradually with time. HSP70 antisense oligodeoxynucleotides 10 μmol/Lfor 72 h inhibited the protective effects of TP at 44 oC on apoptosis of CGNs induced by repolarization. CONCLUSION: HSP70 is involved in protective effects of thermal preconditioning on apoptosis in cerebellar granule neurons induced by repolarization.

关键词： thermal preconditioning heat heat shock proteins cerebellum neurons apoptosis antisense oligodeoxynucleotides Western blotting

Doxepin protects cultured neurons against oxidative stress-induced injury

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Acta Pharmacologica Sinica 2004年第3期25卷 43-46页

作者： Bian-sheng JI,He JI1,Guo-qing LIU2 Department of Pharmacology,China Pharmaceutical University,Nanjing 210009 1Department of Medicine,Henan University,Kaifeng 475001,China Department of Pharmacology China Pharmaceutical University Department of Medicine Henan University

AIM: To investigate protective effects of doxepin (Dox) on cultured neuronal injury induced by oxidative stress. METHODS: Cytotoxicities of glutamate (Glu 0.5 mmol/L, 15 min), sodium dithionite (0.5 mmol/L, 24 h) or hemo- globin (Hb100 mg/L,24 h)and the protective effects of Dox were observed. RESULTS: Exposure of cultured neurons to Glu, sodium dithionite and Hb developed a neurotoxicity expressed in the thiazol blue tetrazolium bro- mide (MTT) assay, the increase of lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) content and intracellular [Ca2+]i accumulation, as well as the decrease of superoxide dismutase (SOD) activity. DOX 1-100 nmol/L significantly inhibited all above changes. CONCLUSION: Dox protects cultured neurons against oxidative stress-induced injury by suppressing intracellular [Ca2+]iaccumulation, decreasing lipid peroxide generation and stimulating antioxidant enzyme.

关键词： doxepin ischemia glutamic acid hemoglobins neurons

Breakup of Spiral Waves in Coupled Hindmarsh-Rose neurons

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Chinese Physics Letters 2008年第12期25卷 4325-4328页

作者：马军贾亚唐军杨利建 Department of Physics Central China Normal University Wuhan 430079 School of Sciences Lanzhou University of Technology Lanzhou 730050

Breakup of spiral wave in the Hindmarsh-Rose neurons with nearest-neighbour couplings is reported. Appropriate initial values and parameter regions are selected to develop a stable spiral wave and then the Gaussian coloured noise with different intensities and correlation times is imposed on all neurons to study the breakup of spiral wave, respectively. Based on the mean field theory, the statistical factor of synchronization is defined to analyse the evolution of spiral wave. It is found that the stable rotating spiral wave encounters breakup with increasing intensity of Gaussian coloured noise or decreasing correlation time to certain threshold.

关键词： NEAREST neighbor analysis (Statistics) RANDOM noise theory neurons MEAN field theory SYNCHRONIZATION CORRELATION (Statistics)

Develop a 3D neurological disease model of human cortical glutamatergic neurons using micropillar-based scaffolds

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Acta Pharmaceutica Sinica B 2019年第3期9卷 557-564页

作者： Cheng Chen Xin Dong Kai-Heng Fang Fang Yuan Yao Hu Min Xu Yu Huang Xixiang Zhang Danjun Fang Yan Liu Institute for Stem Cell and Neural Regeneration School of PharmacyNanjing Medical UniversityNanjing211166China Key Laboratory of Targeted Intervention of Cardiovascular Disease Collaborative Innovation Center for Cardiovascular DiseaseTranslational MedicineSchool of PharmacyNanjing Medical UniversityNanjing211166China Department of Biological Engineering Utah State UniversityLoganUT84322USA Physical Sciences and Engineering Division(PSE) King Abdullah University of Science and TechnologyThuwal23955-6900Kingdomof Saudi Arabia Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing100101China

Establishing an effective three-dimensional(3D) in vitro culture system to better model human neurological diseases is desirable, since the human brain is a 3D structure. Here, we demonstrated the development of a polydimethylsiloxane(PDMS) pillar-based 3D scaffold that mimicked the 3D microenvironment of the brain. We utilized this scaffold for the growth of human cortical glutamatergic neurons that were differentiated from human pluripotent stem cells. In comparison with the 2D culture, we demonstrated that the developed 3D culture promoted the maturation of human cortical glutamatergic neurons by showing significantly more MAP2 and less Ki67 expression. Based on this 3D culture system,we further developed an in vitro disease-like model of traumatic brain injury(TBI), which showed a robust increase of glutamate-release from the neurons, in response to mechanical impacts, recapitulating the critical pathology of TBI. The increased glutamate-release from our 3D culture model was attenuated by the treatment of neural protective drugs, memantine or nimodipine. The established 3D in vitro human neural culture system and TBI-like model may be used to facilitate mechanistic studies and drug screening for neurotrauma or other neurological diseases.

关键词： 3D culture Cortical glutamatergic neurons Human pluripotent stem cells Cell differentiation Disease modeling Traumatic brain injury Neural protective drugs Drug screening

Role of lipids in the control of autophagy and primary cilium signaling in neurons

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Neural Regeneration Research 2024年第2期19卷 264-271页

作者： María Paz Hernández-Cáceres Daniela Pinto-Nuñez Patricia Rivera Paulina Burgos Francisco Díaz-Castro Alfredo Criollo Maria Jose Yañez Eugenia Morselli Instituto de Investigación en Ciencias Odontológicas(ICOD) Facultad de OdontologíaUniversidad de ChileSantiagoChile Department of Basic Sciences Faculty of Medicine and ScienceUniversidad San SebastiánSantiagoChile Physiology Department Faculty of Biological SciencesPontificia Universidad Católica de ChileSantiagoChile Advanced Center for Chronic Diseases(ACCDiS) Facultad de Ciencias Químicas y Farmacéuticas&Facultad de MedicinaUniversidad de ChileSantiagoChile Autophagy Research Center SantiagoChile

The brain is,after the adipose tissue,the organ with the greatest amount of lipids and diversity in their composition in the human *** neurons,lipids are involved in signaling pathways controlling autophagy,a lysosome-dependent catabolic process essential for the maintenance of neuronal homeostasis and the function of the primary cilium,a cellular antenna that acts as a communication hub that transfers extracellular signals into intracellular responses required for neurogenesis and brain development.A crosstalk between primary cilia and autophagy has been established;however,its role in the control of neuronal activity and homeostasis is barely *** this review,we briefly discuss the current knowledge regarding the role of autophagy and the primary cilium in *** we review the recent literature about specific lipid subclasses in the regulation of autophagy,in the control of primary cilium structure and its dependent cellular signaling in physiological and pathological conditions,specifically focusing on neurons,an area of research that could have major implications in neurodevelopment,energy homeostasis,and neurodegeneration.

关键词： autophagic flux cholesterol fatty acids GPCR lysosomal storage diseases neurons NPC1 phosphoinositides primary cilium

Small interfering RNA delivery to the neurons near the amyloid plaques for improved treatment of Alzheimer’s disease

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Acta Pharmaceutica Sinica B 2019年第3期9卷 590-603页

作者： Qian Guo Xiaoyao Zheng Peng Yang Xiaoying Pang Kang Qian Pengzhen Wang Shuting Xu Dongyu Sheng Liuchang Wang Jinxu Cao Wei Lu Qizhi Zhang Xinguo Jiang Key Laboratory of Smart Drug Delivery Ministry of Education & State Key Laboratory of Molecular Engineering of Polymers School of Pharmacy Fudan University

Gene therapy represents a promising treatment for the Alzheimer’s disease(AD). However,gene delivery specific to brain lesions through systemic administration remains big challenge. In our previous work, we have developed an siRNA nanocomplex able to be specifically delivered to the amyloid plaques through surface modification with both CGN peptide for the blood–brain barrier(BBB)penetration and QSH peptide for β-amyloid binding. But, whether the as-designed nanocomplex could indeed improve the gene accumulation in the impaired neuron cells and ameliorate AD-associated symptoms remains further study. Herein, we prepared the nanocomplexes with an siRNA against β-site amyloid precursor protein-cleaving enzyme 1(BACE1), the rate-limiting enzyme of Aβ production, as the therapeutic siRNA of AD. The nanocomplexes exhibited high distribution in the Aβ deposits-enriched hippocampus, especially in the neurons near the amyloid plaques after intravenous administration. In APP/PS1 transgenic mice, the nanocomplexes down-regulated BACE1 in both mRNA and protein levels,as well as Aβ and amyloid plaques to the level of wild-type mice. Moreover, the nanocomplexes significantly increased the level of synaptophysin and rescued memory loss of the AD transgenic mice without hematological or histological toxicity. Taken together, this work presented direct evidences that the design of precise gene delivery to the AD lesions markedly improves the therapeutic outcome.

关键词： siRNA delivery neurons Amyloid plaques BACE1 gene Alzheimer’s disease

Effect of channel block on the collective spiking activity of coupled stochastic Hodgkin-Huxley neurons

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Science China Chemistry 2008年第4期51卷 341-346页

作者： GONG YuBing XU Bo MA XiaoGuang HAN JiQu School of Physics&Electronic Engineering Ludong UniversityYantai 264025China School of Photoelectricity Information Science Technology Yantai UniversityYantai 264005China

Toxins, such as tetraethylammonium (TEA) and tetrodotoxin (TTX), can make potassium or sodium ion channels poisoned, respectively, and hence reduce the number of working ion channels and lead to the diminishment of conductance. In this paper, we have studied by numerical simulations the effects of sodium and potassium ion channel poisoning on the collective spiking activity of an array of coupled stochastic Hodgkin-Huxley (HH) neurons. It is found for a given number of neurons sodium or potas- sium ion channel block can either enhance or reduce the collective spiking regularity, depending on the membrane patch size. For a given smaller or larger patch size, potassium and sodium ion channel block can reduce or enhance the collective spiking regularity, but they have different patch size ranges for the transformation. This result shows that sodium or potassium ion channel block might have dif- ferent effects on the collective spiking activity in coupled HH neurons from the effects for a single neuron, which represents the interplay among the diminishment of maximal conductance and the in- crease of channel noise strength due to the channel blocks, as well as the bi-directional coupling be- tween the neurons.

关键词： neurons ion channel poisoning channel noise kinetics stochastic process

Mitochondrial division inhibitor 1 protects cortical neurons from excitotoxicity:a mechanistic pathway

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Neural Regeneration Research 2018年第9期13卷 1552-1560页

作者： Kuai Zhou Hai-Yuan Yang Peng-Yu Tang Wei Liu Yong-Jun Luo Bin Lv Jian Yin Tao Jiang Jian Chen Wei-Hua Cai Jin Fan Department of Orthopedics First Affiliated Hospital of Nanjing Medical University Department of Orthopedics Ben Q Hospital Affiliated to Nanjing Medical University Department of Orthopedics Affiliated Jiangning Hospital of Nanjing Medical University

Mitochondrial division inhibitor 1（Mdivi-1） is a selective cell-permeable inhibitor of dynamin-related protein-1（Drp1） and mitochondrial *** investigate the effect of Mdivi-1 on cells treated with glutamate,cerebral cortex neurons isolated from neonatal rats were treated with 10 m M glutamate for 24 *** cultured cells and dimethyl sulfoxide-cultured cells were considered as *** cells were detected by flow *** in mitochondrial morphology were examined by electron ***1,Bax,and casp ase-3 expression was evaluated by western blot assays and *** membrane potential was detected using the JC-1 ***-four hours after 10 m M glutamate treatment,Drp1,Bax and caspase-3 expression was upregulated,Drp1 and Bax were translocated to mitochondria,mitochondrial membrane potential was decreased and the rate of apoptosis was *** effects were inhibited by treatment with 50 μM Mdivi-1 for 2 *** finding indicates that Mdivi-1 is a candidate neuroprotective drug that can potentially mitigate against neuronal injury caused by glutamate-induced excitotoxicity.

关键词： nerve regeneration mitochondrial division inhibitor 1 neurons apoptosis mitochondria division dynamin-related protein-I phospho-dynamin-related protein-1 Bax glutamate colocalization neural regeneration

Identification of potential candidate proteins for reprogramming spinal cord-derived astrocytes into neurons:a proteomic analysis

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Neural Regeneration Research 2021年第11期16卷 2257-2263页

作者： Wen-Hao Chen Yu-Xiang Lin Ling Lin Bao-Quan Zhang Shu-Xia Xu Wei Wang Department of Pediatric Surgery Fujian Maternity and Child Health HospitalAffiliated Hospital of Fujian Medical UniversityFuzhouFujian ProvinceChina Department of Breast Surgery Affiliated Union HospitalFujian Medical UniversityFuzhouFujian ProvinceChina Institutes of Biomedical Sciences of Shanghai Medical School Fudan UniversityShanghaiChina Department of Neonatology Fujian Maternity and Child Health HospitalAffiliated Hospital of Fujian Medical UniversityFuzhouFujian ProvinceChina Department of Pathology Fujian Maternity and Child Health HospitalAffiliated Hospital of Fujian Medical UniversityFuzhouFujian ProvinceChina Department of Anatomy and Histoembryology Fujian Medical UniversityFuzhouFujian ProvinceChina

Our previous study has confirmed that astrocytes overexpressing neurogenic differentiation factor 1(NEUROD1)in the spinal cord can be reprogrammed into neurons under in vivo ***,whether they can also be reprogrammed into neurons under in vitro conditions remains unclear,and the mechanisms of programmed conversion from astrocytes to neurons have not yet been *** the present study,we prepared reactive astrocytes from newborn rat spinal cord astrocytes using the scratch method and infected them with lentivirus carrying *** results showed that NEUROD1 overexpression reprogrammed the cultured reactive astrocytes into neurons in vitro with an efficiency of 13.4%.Using proteomic and bioinformatic analyses,1952 proteins were identified,of which 92 were differentially *** these proteins,11 were identified as candidate proteins in the process of reprogramming based on their biological functions and fold-changes in the bioinformatic ***,western blot assay revealed that casein kinase II subunit alpha(CSNK2A2)and pinin(PNN)expression in NEUROD1-overexpressing reactive astrocytes was significantly increased,suggesting that NEUROD1 can directly reprogram spinal cord-derived reactive astrocytes into neurons in vitro,and that the NEUROD1-CSNK2A2-PNN pathway is involved in this *** study was approved by the Animal Ethics Committee of Fujian Medical University,China(approval No.2016-05)on April 18,2016.

关键词： astrocytes glial cells label-free proteomic analysis mechanism neurons primary culture reprogramming spinal cord injury