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Apolipoprotein E4 interferes with lipid metabolism to exacerbate depression-like behaviors in 5xFAD mice

Animal models and Experimental medicine 2024年第3期7卷 347-361页

作者： Yanju Gong mingfeng Li min Liu Xinghan Wu Yanhong Li Chuan Qin Ling Zhang iNHC Key Laboratory of Human Disease Comparative medicine Beijing Engineering Research Center for Experimental Animal Models of Human Critical DiseasesInternational Center for Technology and lnnovation of Animal ModelComparative Medicine CenterInstitute of Laboratory Animal SciencesChinese Academy of Medical Sciences(CAMS)and Peking Union Medical College(PuMC)BeijingChina Changping National Laboratory(CPNL) BeijingChina

Background:Apolipoprotein E4(ApoE4)allele is the strongest genetic risk factor for late-onset Alzheimer's disease,and it can aggravate depressive symptoms in non-AD patients.However,the impact of ApoE4 on AD-associated depression-l ike behaviors and its underlying pathogenic mechanisms remain unclear.methods:This study developed a 5xFAD mouse model overexpressing human ApoE4(E4FAD).Behavioral assessments and synaptic function tests were conducted to explore the effects of ApoE4 on cognition and depression in 5xFAD mice.Changes in peripheral and central lipid metabolism,as well as the levels of serotonin(5-HT)andγ-aminobutyric acid(GABA)neurotransmitters in the prefrontal cortex,were examined.in addition,the protein levels of 24-dehydrocholesterol reductase/glycogen synthase kinase-3 beta/mammalian target of rapamycin(DHCR24/GSK3β/m TOR)and postsynaptic density protein 95/calmodulin-dependent protein kinase ii/brain-derived neurotrophic factor(PSD95/CamK-ii/BDNF)were measured to investigate the molecular mechanism underlying the effects of ApoE4 on AD mice.Results:Compared with 5xFAD mice,E4FAD mice exhibited more severe depressionlike behaviors and cognitive impairments.These mice also exhibited increased amyloid-beta deposition in the hippocampus,increased astrocyte numbers,and decreased expression of depression-related neurotransmitters 5-HT and GABA in the prefrontal cortex.Furthermore,lipid metabolism disorders were observed in E4FAD,manifesting as elevated low-density lipoprotein cholesterol and reduced high-density lipoprotein cholesterol in peripheral blood,decreased cholesterol level in the prefrontal cortex,and reduced expression of key enzymes and proteins related to cholesterol synthesis and homeostasis.Abnormal expression of proteins related to the DHCR24/GSK3β/m TOR and PSD95/CamK-ii/BDNF pathways was also observed.Conclusion:This study found that ApoE4 overexpression exacerbates depressionlike behaviors in 5xFAD mice and confirmed that ApoE4 reduces cognitive function in these mice.The mechanism may

关键词： 5xFAD mice Alzheimer's disease ApoE4 allele depression like

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Comparison of the replication and neutralization of different SARS-CoV-2 Omicron subvariants in vitro

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Animal models and Experimental medicine 2023年第1期6卷 51-56页

作者： Yaqing Zhang Qi Lv Feifei Qi Fengdi Li Ran Deng Xujian Liang mingya Liu Yiwei Yan Linlin Bao Beijing Key Laboratory for Animal models of Emerging and Reemerging infectious Diseases NHC Key Laboratory of Human Disease Comparative MedicineInstitute of Laboratory Animal SciencesChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijingChina National Center of Technology innovation for Animal model BeijingChina

Background:New Omicron subvariants are emerging rapidly from BA.1 to BA.4 and BA.5.Their pathogenicity has changed from that of wild-type(WH-09)and Omicron variants have over time become globally dominant.The spike proteins of BA.4 and BA.5 that serve as the target for vaccine-induced neutralizing antibodies have also changed compared to the previous subvariants,which is likely to cause immune es-cape and the reduction of the protective effect of the vaccine.Our study addresses the above issues and provides a basis for formulating relevant prevention and control strategies.methods:We collected cellular supernatant and cell lysates and measured the viral titers,viral RNA loads,and E subgenomic RNA(E sgRNA)loads in different Omicron subvariants grown in Vero E6 cells,using WH-09 and Delta variants as a reference.Additionally,we evaluated the in vitro neutralizing activity of different Omicron sub-variants and compared it to the WH-09 and Delta variants using macaque sera with different types of immunity.Results:As the SARS-CoV-2 evolved into Omicron BA.1,the replication ability in vitro began to decrease.Then with the emergence of new subvariants,the replication ability gradually recovered and became stable in the BA.4 and BA.5 subvariants.in WH-09-inactivated vaccine sera,geometric mean titers of neutralization antibodies against different Omicron subvariants declined by 3.7~15.4-fold compared to those against WH-09.in Delta-inactivated vaccine sera,geometric mean titers of neutrali-zation antibodies against Omicron subvariants declined by 3.1~7.4-fold compared to those against Delta.Conclusion:According to the findings of this research,the replication efficiency of all Omicron subvariants declined compared with WH-09 and Delta variants,and was lower in BA.1 than in other Omicron subvariants.After two doses of inactivated(WH-09 or Delta)vaccine,cross-neutralizing activities against various Omicron subvariants were seen despite a decline in neutralizing titers.

关键词： cross-neutralize Omicron replication SARS-CoV-2

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Overexpression of ACE2 ameliorates Aβ-induced blood–brain barrier damage and angiogenesis by inhibiting NF-κB/VEGF/VEGFR2 pathway

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Animal models and Experimental medicine 2023年第3期6卷 237-244页

作者： Xueling Zhang Yu Zhang Ling Zhang Chuan Qin institute of Laboratory Animal Sciences CAMS&PUMCBeijingChina National Human Diseases Animal model Resource Center BeijingChina NHC Key Laboratory of Human Disease Comparative medicine BeijingChina Changping National Laboratory(CPNL) BeijingChina

Background:Pathological angiogenesis and blood–brain barrier damage may play an important role in Alzheimer's disease(AD).ACE2 is mainly expressed on the surface of endothelial cells in brain.Recent studies have shown that the expression of ACE2 in AD is reduced,but its role in AD is still unclear.method:We induced AD damage in endothelial cells using Aβ25-35 and overexpressed ACE2 in bEend.3 cells through lentiviral transfection.We detected the effect of Aβ25-35 on cell viability using the CCK-8 assay and examined the effect of overexpressing ACE2 on angiogenesis using an angiogenesis assay.We used western blot and cell immunofluorescence to detect changes in the expression of the VEGF/VEGFR2 pathway,tight junction protein,and NF-κB pathway.Results:Aβ25-35 treatment significantly decreased the expression of ACE2 and reduced cell viability.ACE2 overexpression(1)reduced the number of branches and junctions in tube formation,(2)inhibited the activation of the VEGF/VEGFR2 pathway induced by Aβ25-35,(3)increased the expression of TJPs,including ZO-1 and claudin-5,and(4)restored Aβ25-35-induced activation of the NF-κB pathway.Conclusion:Overexpression of ACE2 can improve pathological angiogenesis and blood–brain barrier damage in AD models in vitro by inhibiting NF-κB/VEGF/VEGFR2 pathway activity.ACE2 may therefore represent a therapeutic target for endothelial cell dysfunction in AD.

关键词： ACE2 Alzheimer's disease angiogenesis blood-brain barrier VEGF

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Breast cancer:an up-to-date review and future perspectives

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Cancer Communications 2022年第10期42卷 913-936页

作者： Ruoxi Hong Binghe Xu Department of medical Oncology Sun Yat-Sen University Cancer CenterState Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangzhouGuangdong 510060P.R.China State Key Laboratory of molecular Oncology and Department of medical Oncology Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100006P.R.China

Breast cancer is the most common cancer worldwide.The occurrence of breast cancer is associated with many risk factors,including genetic and hereditary predisposition.Breast cancers are highly heterogeneous.Treatment strategies for breast cancer vary by molecular features,including activation of human epidermal growth factor receptor 2(HER2),hormonal receptors(estrogen receptor[ER]and progesterone receptor[PR]),gene mutations(e.g.,mutations of breast cancer 1/2[BRCA1/2]and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha[PiK3CA])and markers of the immune microenvironment(e.g.,tumor-infiltrating lymphocyte[TiL]and programmed death-ligand 1[PDL1]).Early-stage breast cancer is considered curable,for which local-regional therapies(surgery and radiotherapy)are the cornerstone,with systemic therapy given before or after surgery when necessary.Preoperative or neoadjuvant therapy,including targeted drugs or immune checkpoint inhibitors,has become the standard of care for most early-stage HER2-positive and triple-negative breast cancer,followed by risk-adapted post-surgical strategies.For ER-positive early breast cancer,endocrine therapy for 5-10 years is essential.Advanced breast cancer with distant metastases is currently considered incurable.Systemic therapies in this setting include endocrine therapy with targeted agents,such as CDK4/6 inhibitors and phosphoinositide 3-kinase(Pi3K)inhibitors for hormone receptor-positive disease,anti-HER2 targeted therapy for HER2-positive disease,poly(ADP-ribose)polymerase inhibitors for BRCA1/2 mutation carriers and immunotherapy currently for part of triple-negative disease.innovation technologies of precision medicine may guide individualized treatment escalation or de-escalation in the future.in this review,we summarized the latest scientific information and discussed the future perspectives on breast cancer.

关键词： PiK3CA Breast cancer

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Characteristics of animal models for COViD-19

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Animal models and Experimental medicine 2022年第5期5卷 401-409页

作者： Feifei Qi Chuan Qin Beijing Key Laboratory for Animal models of Emerging and Reemerging infectious Diseases NHC Key Laboratory of Human Disease Comparative MedicineInstitute of Laboratory Animal ScienceChinese Academy of Medical Sciences and Comparative Medicine CenterPeking Union Medical CollegeBeijingChina National Center of Technology innovation for Animal model BeijingChina

Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)is the causative agent of coronavirus disease 2019(COViD-19),the most consequential pandemic of this century,threatening human health and public safety.SARS-CoV-2 has been continuously evolving through mutation of its genome and variants of concern have emerged.The World Health Organization R&D Blueprint plan convened a range of expert groups to develop animal models for COViD-19,a core requirement for the prevention and control of SARS-CoV-2 pandemic.The animal model construction techniques developed during the SARS-CoV and mERS-CoV pandemics were rapidly deployed and applied in the establishment of COViD-19 animal models.To date,a large number of animal models for COViD-19,including mice,hamsters,minks and nonhuman primates,have been established.infectious diseases produce unique mani-festations according to the characteristics of the pathogen and modes of infection.Here we classified animal model resources around the infection route of SARS-CoV-2,and summarized the characteristics of the animal models constructed via transnasal,localized,and simulated transmission routes of infection.

关键词： animal model characteristics establishment SARS-CoV-2

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Lymphatic metastasis in non-small cell lung cancer: recent discoveries and novel therapeutic targets

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Cancer Communications 2022年第12期42卷 1403-1406页

作者： Xiayao Diao Chao Guo Shanqing Li Department of Thoracic Surgery Peking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730P.R.China

1 LYmPHATiC mETASTASiS AND LYmPHANGiOGENESiS iN NON-SmALL CELL LUNG CANCER Lung cancer is the 2nd most common and 1st deadliest cancer worldwide[1].it presents an enormous burden on society in china,because of its high incidence andmortality rate[2,3].About 80%-85%of lung cancers are non-small cell lung cancer(NSCLC).Lymphatic metastasis is a critical event in disease progression that influences clinical treatment and determines the prognosis for NSCLC[4].

关键词： metastasis lung cancer

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Overexpressed PKm2 promotes macrophage phagocytosis and atherosclerosis

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Animal models and Experimental medicine 2023年第2期6卷 92-102页

作者： Xiaochen Gai Fangming Liu Yuting Wu Baohui Zhang Bufu Tang Kezhuo Shang Lianmei Wang Haihong Zhang Yixin Chen Shuhui Yang Weiwei Deng Peng Li Jing Wang Hongbing Zhang State Key Laboratory of medical molecular Biology Department of PhysiologyInstitute of Basic Medical Sciences and School of Basic MedicineChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina Department of Physiology School of Life ScienceChina Medical UniversityShenyangChina Department of Radiology Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhouChina institute of Chinese materia medica China Academy of Chinese Medical SciencesBeijingChina Department of Cardiac Surgery Fuwai HospitalStata Key Laboratory of Cardiovascular DiseaseNational Center for Cardiovascular Diseases of ChinaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina School of Life Sciences Westlake UniversityHangzhouChina State Key Laboratory of medical molecular Biology Department of PathophysiologyInstitute of Basic Medical Sciences and School of Basic MedicineChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina

Background:The expression of pyruvate kinase muscle 2(PKm2)is augmented in macrophages of patients with atherosclerotic coronary artery disease.The role of PKm2 in atherosclerosis is to be determined.methods:Global and myeloid cell-specific PKm2 knock-in mice with ApoE^(-/-)background(ApoE^(-/-),PKm2^(Ki/Ki)and Lyz2-cre,ApoE^(-/-),and PKm2^(flox/flox))were produced to evaluate the clinical significance of PKm2 in atherosclerosis development.Wild-type and PKm2 knock-in macrophages were isolated to assess the function of PKm2 in macrophage phagocytosis.Atherosclerotic mice were treated with PKm2 inhibitor shikonin(SKN)to evaluate the therapeutic potential of PKm2 suppression in atherosclerosis.Results:Oxidized low-density lipoprotein(oxLDL)upregulated PKm2 in macrophages.PKm2 in return promoted the uptake of oxLDL by macrophages.Overexpressed PKm2 accelerated atherosclerosis in mice.SKN blocked the progress of mouse atherosclerosis.Conclusions:PKm2 accelerates macrophage phagocytosis and atherosclerosis.Targeting PKm2 is a potential therapy for atherosclerosis.

关键词： atherosclerosis low-density lipoprotein macrophage pyruvate kinase muscle 2

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A non-metabolic function of hexokinase 2 in small cell lung cancer:promotes cancer cell stemness by increasing USP11-mediated CD133 stability

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Cancer Communications 2022年第10期42卷 1008-1027页

作者： Juhong Wang Fei Shao Yannan Yang Wei Wang Xueying Yang Renda Li Hong Cheng Sijin Sun Xiaoli Feng Yibo Gao Jie He Zhimin Lu Department of Thoracic Surgery National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China State Key Laboratory of molecular Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China Laboratory of Translational medicine National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China Department of medical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China Department of Pathology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021P.R.China Central Laboratory National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital&Shenzhen HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeShenzhenGuangdong 518116P.R.China Zhejiang Provincial Key Laboratory of Pancreatic Disease The First Affiliated Hospital and Institute of Translational MedicineZhejiang University School of MedicineHangzhouZhejiang 310029P.R.China Cancer Center Zhejiang UniversityHangzhouZhejiang 310029P.R.China

Background:maintenance of cancer stem-like cell(CSC)stemness supported by aberrantly regulated cancer cell metabolism is critical for CSC self-renewal and tumor progression.As a key glycolytic enzyme,hexokinase 2(HK2)plays an instrumental role in aerobic glycolysis and tumor progression.However,whether HK2 directly contribute to CSC stemness maintenance in small cell lung cancer(SCLC)is largely unclear.in this study,we aimed to investgate whether HK2 independent of its glycolytic activity is directly involved in stemness maintenance of CSC in SCLC.methods:immunoblotting analyses were conducted to determine the expression of HK2 in SCLC CSCs and their differentiated counterparts.CSC-like properties and tumorigenesis of SCLC cells with or without HK2 depletion or overexpression were examined by sphere formation assay and xenograft mouse model.immunoprecipitation and mass spectrometry analyses were performed to identify the binding proteins of CD133.The expression levels of CD133-associated and CSC-relevant proteins were evaluated by immunoblotting,immunoprecipitation,immunofluorescence,and immunohistochemistry assay.RNA expression levels of Nanog,POU5F1,Lin28,HK2,Prominin-1 were analyzed through quantitative reverse transcription PCR.Polyubiquitination of CD133 was examined by in vitro or in vivo ubiquitination assay.CD133+cells were sorted by flow cytometry using an anti-CD133 antibody.Results:We demonstrated that HK2 expression was much higher in CSCs of SCLC than in their differentiated counterparts.HK2 depletion inhibited CSC stemness and promoted CSC differentiation.mechanistically,nonmitochondrial HK2 directly interacted with CD133 and enhanced CD133 expression without affecting CD133 mRNA levels.The interaction of HK2 and CD133 promoted the binding of the deubiquitinase ubiquitin-specific protease 11(USP11)to CD133,thereby inhibiting CD133 polyubiquitylation and degradation.HK2-mediated upregulation of CD133 expression enhanced the expression of cell renewal regulators,SCLC cell stemness,and tumor grow

关键词： HK2 metabolic enzyme non-metabolic function cancer stem-like cell CD133 USP11 ubiquitylation SCLC

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Comprehensive analysis of the prognostic impact and immune implication of KiAA1429 in lung adenocarcinoma

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Cancer innovation 2022年第4期1卷 328-343页

作者： Lei Guo Qilin Huai Bolun Zhou Jianming Ying Wei Guo Department of Pathology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingThe People's Republic of China Department of Thoracic Surgery National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingThe People's Republic of China Key Laboratory of minimally invasive Therapy Research for Lung Cancer Chinese Academy of Medical SciencesBeijingThe People's Republic of China

Background:Lung adenocarcinoma(LUAD)is the most common lung cancer worldwide.N6-methyladenosine(m6A)methylation is a messenger RNA(mRNA)modification that plays a key role in tumor growth,immune microenvironment,and immunotherapy response.This study investigated the expression level,mutation status,prognostic value,and predictive ability for response to anti-PD-1 immunotherapy of the m6A methyltransferase KiAA1429 in LUAD.methods:This study examined multiple public data cohorts and independent samples from National Cancer Center(NCC)to evaluate the clinical significance and prognostic value of KiAA1429 in LUAD using bioinformatics techniques and immunohistochemical staining.We also evaluated the predictive value of KiAA1429 expression for anti-PD-1 immunotherapy efficacy.GSEA analysis was performed using KiAA1429 RNA-seq data at the tumor tissue level and cellular level to explore the potential molecular mechanism.Results:in public databases,KiAA1429 was significantly associated with clinicopathological parameters in LUAD patients and had the potential to predict patient prognosis.The mutation characteristics of KiAA1429-related genes were analyzed and TP53,TTN,CSmD3,and other genes showed high mutation frequencies in LUAD.An independent cohort of 415 samples confirmed that high KiAA1429 expression was significantly associated with poorer prognosis in LUAD patients.Analysis of a small immunotherapy cohort showed that patients with high expression of KiAA1429 had better response after immunotherapy,and the proportion of patients with immunotherapy response was higher in this group.Conclusions:Our study confirmed that KiAA1429 was highly expressed in LUAD and was significantly associated with poor prognosis.moreover,KiAA1429 may serve as a potential marker to predict the efficacy of immunotherapy in LUAD.

关键词： KiAA1429 lung adenocarcinoma m6A methylation immunotherapy prognosis

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Sequential immunizations confer cross-protection against variants of SARS-CoV-2,including Omicron in Rhesus macaques

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Signal Transduction and Targeted Therapy 2022年第5期7卷 1746-1755页

作者： Wei Deng Qi Lv Fengdi Li Jiangning Liu Zhiqi Song Feifei Qi Qiang Wei Pin Yu mingya Liu Shasha Zhou Yaqing Zhang Hong Gao Nan Wang Zijing Jia Kai Gao Jiayi Liu Chong Xiao Haiquan Shang Xiangxi Wang Linlin Bao Chuan Qin Beijing Key Laboratory for Animal models of Emerging and Remerging infectious Diseases NHC Key Laboratory of Human Disease Comparative MedicineInstitute of Laboratory Animal ScienceChinese Academy of Medical Sciences and Comparative Medicine CenterPeking Union Medical CollegeBeijing 100021China National Center of Technology innovation for Animal model BeijingChina CAS Key Laboratory of infection and immunity National Laboratory of MacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China Department of Radiology Beijing Anzhen HospitalCapital Medical UniversityBeijingChina

Variants of concern(VOCs)like Delta and Omicron,harbor a high number of mutations,which aid these viruses in escaping a majority of known SARS-CoV-2 neutralizing antibodies(NAbs).in this study,Rhesus macaques immunized with 2-dose inactivated vaccines(Coronavac)were boosted with an additional dose of homologous vaccine or an RBD-subunit vaccine,or a bivalent inactivated vaccine(Beta and Delta)to determine the effectiveness of sequential immunization.The booster vaccination significantly enhanced the duration and levels of neutralizing antibody titers against wild-type.

关键词： neutral harbor Omi

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