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Heterozygous lipoprotein lipase knockout mice exhibit impaired hematopoietic stem/progenitor cell compartment

Animal Models and Experimental Medicine 2021年第4期4卷 418-425页

作者： Guiying Shi Xinyue Li Keya Li Yiying Huang Xuepei Lei Lin Bai Chuan Qin The Institute of Laboratory Animal Sciences CAMS&PUMCBeijing Engineering Research Center for Experimental Animal Models of Human Critical DiseasesBeijingP.R.China

Background : Hematopoietic stem cells (HSC) maintain the hematopoietic system homeostasis through self- renewal and multilineage differentiation potential. HSC are regulated by the microenvironment, cytokine signaling, and transcription factors. Recent results have shown that lipid pathways play a key role in the regulation of HSC quiescence, proliferation, and division. However, the mechanism by which lipid metabolism regulates HSC proliferation and differentiation remains to be clarified. Lipoprotein lipase (LPL) is an essential enzyme in the anabolism and catabolism of very low- density lipoprotein, chylomicrons, and triglyceride- rich lipoproteins. Methods : The percentage of hematopoietic stem/progenitor cells and immune cells were determined by fluorescence- activated cell sorting (FACS). The function and the mechanism of HSCs were analyzed by cell colony forming assay and qPCR analysis. The changes in LPL^(+/−) HSC microenvironment were detected by transplantation as- says using red fluorescent protein (RFP) transgenic mice. Results : To explore the function of LPL in HSC regulation, heterozygous LPL- knockout mice (LPL^(+/−)) were established and analyzed by FACS. LPL^(+/−) mice displayed decreased hematopoietic stem/progenitor cell compartments. In vitro single- cell clono- genic assays and cell-cycle assays using FACS promoted the cell cycle and increased proliferation ability. qPCR analysis showed the expression of p57^(KIP2) and p21^(WAF1)/ ^(CIP1) in LPL^(+/−) mice was upregulated. Conclusions : LPL^(+/−) mice exhibited HSC compartment impairment due to promotion of HSC proliferation, without any effects on the bone marrow (BM) microenvironment.

关键词： cell cycle HSCs LPL

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Effectiveness and mechanisms of adiposederived stem cell therapy in animal models of Parkinson’s disease:a systematic review and meta-analysis

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Translational Neurodegeneration 2021年第2期10卷 166-177页

作者： Keya Li Xinyue Li Guiying Shi Xuepei Lei Yiying Huang Lin Bai Chuan Qin NHC Key Laboratory of Human Disease Comparative Medicine Beijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious DiseasesInstitute of Laboratory Animal ScienceChinese Academy of Medical Sciences and Comparative Medicine CenterPeking Union Medical CollegeBeijing 100021China

Animal models provide an opportunity to assess the optimal treatment way and the underlying mechanisms of direct clinical application of adipose-derived stem cells(ADSCs).Previous studies have evaluated the effects of primitive and induced ADSCs in animal models of Parkinson’s disease(PD).Here,eight databases were systematically searched for studies on the effects and in vivo changes caused by ADSC intervention.Quality assessment was conducted using a 10-item risk of bias tool.For the subsequent meta-analysis,study characteristics were extracted and effect sizes were computed.Ten out of 2324 published articles(n=169 animals)were selected for further meta-analysis.After ADSC therapy,the rotation behavior(10 experiments,n=156 animals)and rotarod performance(3 experiments,n=54 animals)were improved(P<0.00001 and P=0.0003,respectively).The rotation behavior test reflected functional recovery,which may be due to the neurogenesis from neuronally differentiated ADSCs,resulting in a higher pooled effect size of standard mean difference(SMD)(−2.59;95%CI,−3.57 to−1.61)when compared to that of primitive cells(−2.18;95%CI,−3.29 to−1.07).Stratified analyses by different time intervals indicated that ADSC intervention exhibited a long-term effect.Following the transplantation of ADSCs,tyrosine hydroxylase-positive neurons recovered in the lesion area with pooled SMD of 13.36[6.85,19.86].Transplantation of ADSCs is a therapeutic option that shows long-lasting effects in animal models of PD.The potential mechanisms of ADSCs involve neurogenesis and neuroprotective effects.The standardized induction of neural form of transplanted ADSCs can lead to a future application in clinical practice.

关键词： Parkinson’s disease Adipose-derived stem cells Animal model Stem cell therapy Meta-analysis Neurogenesis Neuroprotection

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Effectiveness and mechanisms of adipose-derived stem cell therapy in animal models of Parkinson's disease:a systematic review and meta-analysis

Effectiveness and mechanisms of adipose-derived stem cell th...

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第十六届中国实验动物科学年会

作者： Keya Li Xinyue Li Guiying Shi Xuepei Lei Yiying Huang Lin Bai Chuan Qin Key Laboratory of Human Disease Comparative Medicine Chinese Ministry of HealthBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious DiseasesInstitute of Laboratory Animal ScienceChinese Academy of Medical Sciencesand Comparative Medicine CenterPeking Union Medical College

Animal models provide an opportunity to assess the optimal treatment way and the underlying mechanisms of direct clinical application of adipose-derived stem cells(ADSCs).Previous studies have evaluated the effects of primitive and induced ADSCs in animal models of Parkinson’s disease(PD).Here,eight databases were systematically searched for studies on the effects and in vivo changes caused by ADSC intervention.Quality assessment was conducted using a 10-item risk of bias tool.For thesubsequent meta-analysis,study characteristics were extracted and effect sizes were computed.Ten outof 2,324 published articles(n=169 animals)were selected for further meta-analysis.After ADSC therapy,the rotation behavior(10 experiments,n=156 animals) and rotarod performance(3 experiments,n=54 animals) were improved(P <0.00001 and P=0.0003,respectively).The rotation behavior test reflects the functional recovery,which may be due to the neurogenesis from neuronally differentiated ADSCs,resulting in a higher pooled effect size of standard mean difference(SMD)(-2.59;95%Cl,-3.57 to-1.61) when compared to that of primitive cells(-2.18;95% Cl,-3.29 to-1.07).Stratified analyses by different time intervals indicated that ADSC intervention exhibited a long-term effect.Following the transplantation of ADSCs,tyrosine hydroxylase-positive neurons recovered in the lesion area with pooled SMD of 13.36[6.85,19.86].Transplantation of ADSCs is a therapeutic option that shows long-lasting effects in animal models of PD.The potential mechanisms of ADSCs involve neurogenesis and neuroprotective effects.The standardized induction of neural form of transplanted ADSCs can lead to a future application in clinical practice.

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VEGFR2 inhibition hampers breast cancer cell proliferation via enhanced mitochondrial biogenesis

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Cancer Biology & Medicine 2021年第1期18卷 139-154页

作者： Hao Ni Min Guo xuepei Zhang lei Jiang Shuai Tan Juan Yuan Huanhuan L Cui Yanan Min Junhao Zhang Susanne Schlisio Chunhong Ma Wangjun Liao Monica Nister Chunlin Chen Shuijie Li Nailin Li Department of Gynaecology and Obstetrics Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China Karolinska Institutet Department of Medicine-SolnaClinical Pharmacology GroupKarolinska University Hospital-SolnaStockholm 17176Sweden Karolinska Institutet Department of Oncology-PathologyBio ClinicumSolna 17164Sweden State Key Laboratory of Bioorganic and Natural Products Chemistry Center for Excellence in Molecular SynthesisShanghai Institute of Organic ChemistryChinese Academy of SciencesShanghai 200032China Department of Pathology Zhejiang Provincial Key Laboratory of PathophysiologyNingbo University School of MedicineNingbo 315211China Department of Hematology Affiliated Hospital of Jining Medical UniversityJining 272000China Department of Cell and Molecular Biology Stockholm 17177Sweden Karolinska Institutet Department of MicrobiologyTumor and Cell BiologyStockholm 17177Sweden Shandong University Cheeloo Medical College School of Basic MedicineDepartment of ImmunologyJinan 250000China Department of Oncology Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China

Objective:Vascular endothelial growth factor(VEGF),apart from its predominant roles in angiogenesis,can enhance cancer cell proliferation,but its mechanisms remain elusive.The purpose of the present study was therefore to identify how VEGF regulates cancer cell proliferation.Methods:VEGF effects on cancer cell proliferation were investigated with the VEGF receptor 2 inhibitor,Ki8751,and the breast cancer cell lines,MCF-7 and MDA-MB-231,using flow cytometry,mass spectrometry,immunoblotting,and confocal microscopy.Data were analyzed using one-way analysis of variance followed by Tukey’s multiple comparison test.Results:VEGF blockade by Ki8751 significantly reduced cancer cell proliferation,and enhanced breast cancer cell apoptosis.Mass spectrometric analyses revealed that Ki8751 treatment significantly upregulated the expression of mitochondrial proteins,suggesting the involvement of mitochondrial biogenesis.Confocal microscopy and flow cytometric analyses showed that Ki8751 treatment robustly increased the mitochondrial masses of both cancer cells,induced endomitosis,and arrested cancer cells in the high aneuploid phase.VEGFR2 knockdown by sh RNAs showed similar effects to those of Ki8751,confirming the specificity of Ki8751 treatment.Enhanced mitochondrial biogenesis increased mitochondrial oxidative phosphorylation and stimulated reactive oxygen species(ROS)production,which induced cancer cell apoptosis.Furthermore,Ki8751 treatment downregulated the phosphorylation of Akt and PGC1α,and translocated PGC1αinto the nucleus.The PGC1αalterations increased mitochondrial transcription factor A(TFAM)expression and subsequently increased mitochondrial biogenesis.Conclusions:VEGF enhances cancer cell proliferation by decreasing Akt-PGC1α-TFAM signaling-mediated mitochondrial biogenesis,ROS production,and cell apoptosis.These findings suggested the anticancer potential of Ki8751 via increased mitochondrial biogenesis and ROS production.

关键词： Breast cancer VEGF VEGFR2 mitochondria TFAM ROS apoptosis

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基于氧化应激与细胞凋亡探究双酚A慢性暴露致小鼠肾毒性作用机制

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生物工程学报 2023年第1期39卷 372-385页

作者：唐中伟王慧敏张卓孔艳彪雷雪配袁建琴山西农业大学生命科学学院山西太谷030801 农业农村部农作物生态环境安全监督检验测试中心(太原) 山西太谷030801

双酚A(bisphenol A,BPA)被广泛应用于生产环氧树脂和聚碳酸酯塑料等制品,在强酸、强碱或高温条件下,BPA被释放出来,然后渗入环境中。在大多数生物液体中都检测到了不同浓度的BPA,BPA的存在已被证明与许多慢性疾病密切相关,包括慢性肾病(... 详细信息

双酚A(bisphenol A,BPA)被广泛应用于生产环氧树脂和聚碳酸酯塑料等制品,在强酸、强碱或高温条件下,BPA被释放出来,然后渗入环境中。在大多数生物液体中都检测到了不同浓度的BPA,BPA的存在已被证明与许多慢性疾病密切相关,包括慢性肾病(chronic kidney disease,CKD)。然而,关于BPA的有害作用及其对CKD的不良影响知之甚少。为了探讨BPA对动物肾毒性的作用机制,本研究通过向饮水中加入0.01、0.1和1 mg/L的BPA,暴露于雌性小鼠4周后,交配和怀孕的雌性小鼠持续接触BPA,直到断奶;F1代3周龄雄性仔鼠继续口服相同剂量的BPA,持续10周。结果表明,0.1mg/L和1mg/LBPA处理组小鼠的肾脏损伤严重,血清中肾脏功能指标尿素氮(urea nitrogen,UN)、肌酐(creatinine,CR)和尿酸(uric acid,UA)的含量均发生显著升高(P<0.05);肾脏组织形态结构被损害;肾脏抗氧化相关基因在mRNA和蛋白水平上的表达显著降低(P<0.05),包括谷胱甘肽硫转移酶(glutathione-S-transferase,GST)、超氧化物歧化酶(superoxide dismutase,SOD)和过氧化氢酶(catalase,CAT);硫代巴比妥酸反应物(thiobarbituric acid reactive substances,TBARS)的含量和凋亡指数(Caspase-3和Bax/Bcl-1的比值)相关基因和蛋白的表达显著增强。以上研究结果证实,氧化应激和细胞凋亡在BPA慢性暴露诱导的动物肾毒性中起着重要作用。

关键词：双酚A 细胞凋亡慢性暴露肾毒性氧化应激

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松南新区小型凹陷油气成藏特征分析——以彰武断陷为例

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海洋石油 2016年第1期36卷 17-22页

作者：李丹于雷樊薛沛中国石油化工股份有限公司东北油气分公司勘探开发研究院吉林长春130026

中石化松辽盆地南部新登记区块(简称松南新区)分布着20多个有效勘探面积100~300 km^2、现今残留厚度小于3 000 m的小型断陷,它们具有相似的成盆、成烃、成藏演化过程。彰武断陷油藏类型及分布规律的研究表明,其成藏具有"低熟近源、陡坡... 详细信息

中石化松辽盆地南部新登记区块(简称松南新区)分布着20多个有效勘探面积100~300 km^2、现今残留厚度小于3 000 m的小型断陷,它们具有相似的成盆、成烃、成藏演化过程。彰武断陷油藏类型及分布规律的研究表明,其成藏具有"低熟近源、陡坡控砂、相带控藏、构造富集"特征,进而建立斜坡带、洼陷带、断阶带成藏模式。

关键词：彰武断陷低熟近源陡坡控砂相带控藏构造富集

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不同物种端粒结合蛋白和端粒酶的研究进展

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中国比较医学杂志 2022年第3期32卷 136-142页

作者：石桂英黄艺滢雷雪裴李欣悦白琳中国医学科学院医学实验动物研究所北京协和医学院比较医学中心国家卫生健康委员会人类疾病比较医学重点实验室国家中医药管理局人类疾病动物模型三级实验室北京100021

端粒位于真核生物染色体末端,在复制过程中保护染色体的完整性。端粒随着细胞的有丝分裂而缩短,端粒酶在胚胎干细胞等细胞中起到了延长端粒的作用。端粒结合蛋白包括shelterin复合体和CST复合体,端粒酶以自身RNA组分为模板逆转录合成端... 详细信息

端粒位于真核生物染色体末端,在复制过程中保护染色体的完整性。端粒随着细胞的有丝分裂而缩短,端粒酶在胚胎干细胞等细胞中起到了延长端粒的作用。端粒结合蛋白包括shelterin复合体和CST复合体,端粒酶以自身RNA组分为模板逆转录合成端粒,端粒结合蛋白和端粒酶在保持端粒长度和稳定中都有重要作用。尽管不同物种中端粒序列类似,但是端粒及端粒酶在生理和/或病理状态下的功能却不尽相关。本文对不同物种的端粒结合蛋白和端粒酶的组成、功能等进行综述,以深入了解端粒生物学功能,为端粒功能障碍相关疾病的治疗提供科学基础。

关键词：端粒 shelterin CST 端粒酶

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Microglial Exosome miR-7239-3p Promotes Glioma Progression by Regulating Circadian Genes

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Neuroscience Bulletin 2021年第4期37卷 497-510页

作者： xuepei Li Junwen Guan Zhou Jiang Shuting Cheng Wang Hou Junjie Yao Zhengrong Wang Ministry of Health Key Laboratory of Chronobiology College of Basic Medicine and Forensic MedicineSichuan UniversityChengdu 610041China Medical Simulation Center Chengdu First People’s HospitalChengdu 610041China Neurosurgery Department West China HospitalSichuan UniversityChengdu 610041China Department of Respiratory and Critical Care Medicine West China HospitalSichuan UniversityChengdu 610041China Department of Anesthesiology Wuhan Third HospitalTongren Hospital of Wuhan UniversityWuhan 410000China

Glioma-associated microglial cells,a key component of the tumor microenvironment,play an important role in glioma progression.In this study,the mouse glioma cell line GL261 and the mouse microglia cell line BV2 were chosen.First,circadian gene expression in glioma cells co-cultured with either M1 or M2 microglia was assessed and the exosomes of M2-polarized and unpolarized BV-2 microglia were extracted.Subsequently,we labeled the exosomes with PKH67 and treated GL261 cells with them to investigate the exosome distribution.GL261 cell phenotypes and related protein expression were used to explore the role of M2 microglial exosomes in gliomas.Then a specific miR-7239-3p inhibitor was added to verify miR-7239-3p functions.Finally,the mouse subcutaneous tumorigenic model was used to verify the tumorigenic effect of M2 microglial exosomes in vivo.Our results showed that in gliomas co-cultured with M2 microglia,the expression of the BMAL1 protein was decreased(P<0.01),while the expression of the CLOCK protein was increased(P<0.05);opposite results were obtained in gliomas co-cultured with M1 microglia.After treatment with M2 microglial exosomes,the apoptosis of GL261 cells decreased(P<0.001),while the viability,proliferation,and migration of GL261 cells increased.Increased expression of N-cadherin and Vimentin,and decreased E-cadherin expression occurred upon treatment with M2 microglial exosomes.Addition of an miR-7239-3p inhibitor to M2 microglial exosomes reversed these results.In summary,we found that miR-7239-3p in the glioma microenvironment is recruited to glioma cells by exosomes and inhibits Bmal1 expression.M2 microglial exosomes promote the proliferation and migration of gliomas by regulating tumor-related protein expression and reducing apoptosis.

关键词： Glioma Microglia Bmal1 Exosome miR-7239-3p

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Preparation of Durable Emitter of Electrospray Mass Spectrometry by Covalently Coating the Fused-Silica Capillary Tip with Carbon-Nanotube Sol-Gel Composite Material

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Chinese Journal of Chemistry 2014年第4期32卷 293-297页

作者： Hanzhi Zhang Chao Liu xuepei Zhang Jingwu Kang Shanghai Institute of Organic Chemistry Chinese Academy of SciencesShanghai 200032China

A simple approach for the preparation of emitter of electrospray ionization mass spectrometry by covalently coating the fused-silica capillary tip with the conductive carbon-nanotube sol-gel composite material(CNTSCM)is described.The CNTSCM was prepared by dispersing single-walled carbon nanotubes in the sol composed of a mixture of 3-glycidoxypropyltrimethoxysilane and 3-aminopropyltrimethoxysilane,and ethanol.The long-term sta-bility of the prepared ESI emitters was demonstrated by at least 180 h of continuous use.Signal intensity obtained by the prepared emitter was mass-flux sensitive when the flow rate was lower than 500 nL/min,while the signal in-tensity performed a concentration dependence when the flow rate was in the range of 500-800 nL/min.The use-fulness of such a prepared emitter was demonstrated by the analysis of various types of samples such as organic small molecular drugs,oligosaccharide,peptide,and protein.

关键词： electrospray emitter mass spectrometry carbon-nanotube sol-gel composite material

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Improving the surface insulating performance of epoxy resin/Al_(2)O_(3)composite materials by extending chain of liquid epoxy resin with Me-THPA

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High Voltage 2020年第4期5卷 472-481页

作者： Yushun Zhao Yuanhan He Kerong Yang xuepei Wang Jinhui Bai Bin Du School of Electrical Engineering and Automation Hefei University of TechnologyBaohe District Tunxi Road No.193HefeiPeople's Republic of China

Basin-type insulators are made by epoxy resin composite materials.Curing defects are easily formed in basin-type insulators,and degrade their insulating performances.High curing exothermic rates of epoxy resin composite materials have deemed as the main cause of curing defects formation.In this study,methyl tetrahydrophthalic anhydride(Me-THPA)was used to extend the molecular chain of liquid epoxy resin to prepare epoxy resin composite materials with low curing exothermic rates.Curing exothermic properties,molecular weight distribution,curing stress,microstructures,and surface flashover characteristics of the composite materials were investigated.The results showed that chain-extended epoxy resin had low curing exothermic rates.The curing stress of the chain-extended epoxy resin composite materials was small.The curing defects forming in the composite materials were inhibited.Negative DC surface flashover characteristics of these composite materials were improved.Furthermore,variation of functional groups of the composite materials was studied before and after surface flashover tests.Results showed that the content of carbon-oxygen single bonds(-C-O)in the chain-extended epoxy resin composite materials was observed to decrease.The-C-O bonds also affect the voltage withstand capability of the epoxy resin composite materials.

关键词： composite materials resin

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