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SARS-CoV-2 immunity in animal models

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Cellular & molecular Immunology 2024年第2期21卷 119-133页

作者： Zhao Chen Yaochang Yuan Qingtao Hu Airu Zhu Fenghua Chen Shu Li Xin Guan Chao Lv Tian Tang Yiyun He Jinling Cheng Jie Zheng Xiaoyu Hu Jingxian Zhao Jincun Zhao Jing Sun State key laboratory of Respiratory Disease National Clinical Research Centre for Respiratory DiseaseNational Centre for Respiratory MedicineGuangzhou Institute of Respiratory Healththe First Affiliated Hospital of Guangzhou Medical UniversityGuangzhouGuangdong 510182China GMU-GIBH Joint School of Life Sciences Guangzhou Medical UniversityGuangzhou 510000China Guangzhou National laboratory GuangzhouGuangdong 510005China Shanghai Institute for Advanced Immunochemical Studies School of Life Science and TechnologyShanghaiTech UniversityShanghai 201210China Institute for Hepatology National Clinical Research Center for Infectious DiseaseShenzhen Third People’s Hospitalthe Second Affiliated HospitalSchool of MedicineSouthern University of Science and TechnologyShenzhen 518005China

The COVID-19 pandemic,which was caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has become a worldwide health crisis due to its ***-CoV-2 infection results in severe respiratory illness and can lead to significant complications in affected *** complications encompass symptoms such as coughing,respiratory distress,fever,infectious shock,acute respiratory distress syndrome(ARDS),and even multiple-organ *** models serve as crucial tools for investigating pathogenic mechanisms,immune responses,immune escape mechanisms,antiviral drug development,and vaccines against ***,various animal models for SARS-CoV-2 infection,such as nonhuman primates(NHPs),ferrets,hamsters,and many different mouse models,have been *** model possesses distinctive features and *** this review,we elucidate the immune response elicited by SARS-CoV-2 infection in patients and provide an overview of the characteristics of various animal models mainly used for SARS-CoV-2 infection,as well as the corresponding immune responses and applications of these models.A comparative analysis of transcriptomic alterations in the lungs from different animal models revealed that the K18-hACE2 and mouse-adapted virus mouse models exhibited the highest similarity with the deceased COVID-19 ***,we highlighted the current gaps in related research between animal model studies and clinical investigations,underscoring lingering scientific questions that demand further clarification.

关键词： COVID-19 SARS-CoV-2 animal models immune response

Fulminant Myocarditis Complicated by Stiff-person Syrndrom A Case Report

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Cardiology Discovery 2024年第2期4卷 183-186页

作者： Peng Chen Nana Tang Huilan Zhang Dao Wen Wang Division of Cardiology Departments of Internal Medicine and Genetic Diagnosis CenterTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China Hubei key laboratory of genetics and molecular Mechanism of Cardiological Disorders WuhanHubei 430030China Department of Respiratory and Critical Care medicine Tongji Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China.

This case report described a 61-year-old woman who presented with dizziness,headache,muscle ache,diplopia,and vomiting who lost *** hospital admission,the levels of high-sensitivity cardiac troponin I and partial pressure of carbon dioxide were increased *** of consciousness occurred twice after removal of invasive ventilator *** angiography demonstrated no stenosis in coronary *** revealed inactivity of respiratory *** disturbance and autonomic-nerve dysfunctions were *** antibody against glutamic acid decarboxylase was *** rare phenotypes of persistent stiffness of muscles in the neck,face,bilateral upper and lower limbs were *** patient was diagnosed with fulminant myocarditis complicated by Stiff-person *** treatment(glucocorticoids and immunoglobulins)elicited satisfactory therapeutic *** this case report,it was found that fulminant myocarditis and Stiff-person syndrome shared a common pathogenesis:"cytokine storm".Such patients may benefit from early treatment with immunomodulatory agents.

关键词： Myocarditis Stiff-person syndrome Cytokine storm Immunomodulating treatment

METTL14 downregulation drives S100A4^(+)monocyte-derived macrophages via MyD88/NF-κB pathway to promote MAFLD progression

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Signal Transduction and Targeted Therapy 2024年第5期9卷 2176-2192页

作者： Yue-fan Wang Wen-li Zhang Zhi-xuan Li Yue Liu Jian Tan Hao-zan Yin Zhi-chao Zhang Xian-jie Piao Min-hao Ruan Zhi-hui Dai Si-jie Wang Chen-yang Mu Ji-hang Yuan Shu-han Sun Hui Liu Fu Yang The Third Department of Hepatic Surgery Eastern Hepatobiliary Surgery Hospital Affiliated to Naval Medical University200438 ShanghaiChina The Department of Medical genetics Naval Medical University200433 ShanghaiChina Translational medicine Research Center Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital100048 BeijingChina The Department of Pharmaceutical Analysis School of PharmacyNaval Medical University200433 ShanghaiChina key laboratory of Biosafety Defense Ministry of Education200433 ShanghaiChina Shanghai key laboratory of Medical Biodefense 200433 ShanghaiChina

Without intervention,a considerable proportion of patients with metabolism‐associated fatty liver disease(MAFLD)will progress from simple steatosis to metabolism‐associated steatohepatitis(MASH),liver fibrosis,and even hepatocellular ***,the molecular mechanisms that control progressive MAFLD have yet to be fully ***,we unraveled that the expression of the N6-methyladenosine(m6A)methyltransferase METTL14 is remarkably downregulated in the livers of both patients and several murine models of MAFLD,whereas hepatocyte-specific depletion of this methyltransferase aggravated lipid accumulation,liver injury,and ***,hepatic Mettl14 overexpression alleviated the above pathophysiological changes in mice fed on a high-fat diet(HFD).Notably,in vivo and in vitro mechanistic studies indicated that METTL14 downregulation decreased the level of GLS2 by affecting the translation efficiency mediated by YTHDF1 in an m6A-depedent manner,which might help to form an oxidative stress microenvironment and accordingly recruit Cx3cr1^(+)Ccr2^(+)monocyte-derived macrophages(Mo-macs).In detail,Cx3cr1^(+)Ccr2^(+)Mo-macs can be categorized into M1-like macrophages and S100A4-positive macrophages and then further activate hepatic stellate cells(HSCs)to promote liver *** experiments revealed that CX3CR1 can activate the transcription of S100A4 via CX3CR1/MyD88/NF-κB signaling pathway in Cx3cr1^(+)Ccr2^(+)*** of METTL14 or GLS2,or interfering with this signal transduction pathway such as inhibiting MyD88 could ameliorate liver injuries and *** together,these findings indicate potential therapies for the treatment of MAFLD progression.

关键词： S100A4 MyD88 metabolism

Multi-omics analyses of G6PD deficiency variants in Chinese population

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Journal of genetics and Genomics 2024年第1期51卷 100-104页

作者： He Ji Jiahuan Chen Peide Huang Zhimin Feng Weining Hu Mengyao Dai Xiaohui Sun Xiao Jin Guangquan Chen Guang Ning Lin Li Weiqing Wang Yanan Cao Department of Endocrine and Metabolic Diseases Shanghai Institute of Endocrine and Metabolic DiseasesNational Clinical Research Centre for Metabolic DiseasesState Key Laboratory of Medical GenomicsResearch Unit of Clinical and Basic Research on Metabolic Diseases of Chinese Academy of Medical SciencesRuijin Yangtze River Delta Health InstituteWuxi Branch of Ruijin HospitalRuijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China National Research Center for Translational medicine National Key Scientific Infrastructure for Translational MedicineShanghai Jiao Tong UniversityShanghai 200240China SJTU-BGI Innovation Research Center Shanghai 200240China BGI-shenzhen ShenzhenGuangdong 518083China

Glucose-6-phosphate dehydrogenase(G6PD)deficiency is one of the most prevalent hereditary and X-linked enzyme disorders caused by the pathogenetic G6PD(NM_001042351.2)variants(Yang et al.,2016).The clinical manifestations of G6PD deficiency offer a wide spectrum of diverse disease phenotypes(Hecker et al.,2013).Investigations of prevalence and molecular epidemiology demonstrate that G6PD deficiency affects over 400 milion individuals worldwide and leads to thousands of deaths annually(Mortality and Causes of Death,2015).

关键词： al. G6PD epidemiology

Perspectives of genetic management strategy for inherited cardiovascular diseases in China

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Chinese Medical Journal 2024年第8期137卷 959-961页

作者： Yaoyao Zhang Yanjiang Zheng Mengyuan Dai Kaiyu Zhou Lijun Fu Yuxuan Guo Yihua He Fen Li Rui Gao Donghui Zhang Xujie Liu Jie Tian Yimin Hua Yifei Li Lang Qin key laboratory of Birth Defects and Related Diseases of Women and Children of MOE West China Second University HospitalSichuan UniversityChengduSichuan 610041China Department of Department of Obstetrics and Gynecology West China Second University HospitalSichuan UniversityChengduSichuan 610041China Department of Pediatrics West China Second University HospitalSichuan UniversityChengduSichuan 610041China Department of Cardiology Shanghai Children’s Medical CenterSchool of MedicineShanghai Jiao Tong UniversityShanghai 200025China Peking University Health Science Center School of Basic Medical SciencesThe Institute of Cardiovascular SciencesKey Laboratory of Molecular Cardiovascular Science of Ministry of EducationBeijing 100191China Department of Ultrasound Beijing Anzhen Hospital affiliated to Capital Medical UniversityBeijing 100029China State key laboratory of Biocatalysis and Enzyme Engineering School of Life ScienceHubei UniversityWuhanHubei 430062China shenzhen key laboratory of Cardiovascular Disease Fuwai Hospital Chinese Academy of Medical SciencesShenzhenGuangdong 518052China Department of Cardiology Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and Disorders(Chongqing)China International Science and Technology Cooperation Base of Child Development and Critical DisordersChildren’s Hospital of Chongqing Medical UniversityChongqing 400014China

Inherited cardiovascular diseases(CVDs)threaten human health and pose an enormous economic burden *** alteration is a major risk factor for many *** disorders are usually controlled by a pair of alleles,affecting offspring according to the Mendelian principle,regardless of isolated primary damage or secondary injury from other syndromes or *** date,there are hundreds of inherited *** advances in nextgeneration sequencing(NGS)technologies,rapid and accurate molecular diagnosis of patients with inherited CVDs is clinically ***,great improvements have been made in recent years,and targeted therapy and assist devices have been used in clinical *** there is still no totally efficient strategy for dealing with inherited ***.

关键词： diagnosis hundreds dealing

维普期刊数据库

SMXL5 attenuates strigolactone signaling in Arabidopsis thaliana by inhibiting SMXL7 degradation

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molecular Plant 2024年第4期17卷 631-647页

作者： Qingtian Li Haiyang Yu Wenwen Chang Sunhyun Chang Michael Guzman Lionel Faure Eva-Sophie Wallner Heqin Yan Thomas Greb Lei Wang Ruifeng Yao David C.Nelson Department of Botany and Plant Sciences University of CaliforniaRiversideRiversideCA 2521USA Yazhouwan National laboratory Sanya 572025China Hainan Seed Industry laboratory Sanya 57205China State key laboratory of Chemo/Biosensing and Chemometrics Hunan Provincial Key Laboratory of Plant Functional Genomics and Developmental RegulationCollege of BiologyHunan UniversityChangsha 410082China key laboratory of Seed Innovation Center for Agricultural Resources ResearchInstitute of Genetics and Developmental BiologyChinese Academy of SciencesShijiazhuangHebei 050021China University of Chinese Academy of Sciences Beijing 10004China School of the Sciences Biology DivisionTexas Woman’s UniversityDentonTX 76204USA Centre for Organismal Studies(COS) Heidelberg University6120 HeidelbergGermany

Hormone-activated proteolysis is a recurring theme of plant hormone signaling *** strigolactone signaling,the enzyme receptor DWARF14(D14)and an F-box protein,MORE AXILLARY GROWTH2(MAX2),mark SUPPRESSOR OF MAX21-LIKE(SMXL)family proteins SMXL6,SMXL7,and SMXL8 for rapid *** of these transcriptional corepressors initiates downstream growth *** homologous proteins SMXL3,SMXL4,and SMXL5,however,are resistant to MAX2-mediated *** discovered that the smxl4 smxl5 mutant has enhanced responses to ***5 attenuates strigolactone signaling by interfering with AtD14-SMXL7 ***5 interacts with AtD14 and SMXL7,providing two possible ways to inhibit SMXL7 ***5 function is partially dependent on an ethylene-responsive-element binding-factor-associated amphiphilic repression(EAR)motif,which typically mediates interactions with the TOPLESS family of transcriptional ***,we found that loss of the EAR motif reduces SMXL5-SMXL7 interactions and the attenuation of strigolactone signaling by *** hypothesize that integration of SMXL5 into heteromeric SMXL complexes reduces the susceptibility of SMXL6/7/8 proteins to strigolactone-activated degradation and that the EAR motif promotes the formation or stability of these *** mechanism may provide a way to spatially or temporally fine-tune strigolactone signaling through the regulation of SMXL5 expression or translation.

关键词： Arabidopsis typically inhibiting

PCAF-mediated acetylation of METTL3 impairs mR NA translation efficiency in response to oxidative stress

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Science China Life Sciences 2024年

作者： Cheng Liu Miao Yu Mengyuan Wang Siyuan Yang Yenan Fu Lei Zhang Chaoyang Zhu Hongquan Zhang Program for Cancer and Cell Biology Department of Human Anatomy Histology and Embryology School of Basic Medical Sciences Peking University International Cancer Institute and State Key Laboratory of Molecular Oncology Peking University Health Science Center Department of General Surgery and Urological Surgery Huaihe Hospital Henan University Department of Human Anatomy Histology and Embryology Shenzhen University School of Medicine

METTL3 methylates RNA and regulates the fate of mRNA through its methyltransferase activity. METTL3 enhances RNA translation independently of its catalytic activity. However, the underlying mechanism is still elusive. Here, we report that METTL3 is both interacted with and acetylated at lysine 177 by the acetyltransferase PCAF and deacetylated by SIRT3. Neither the methyltransferase activity nor the stability of METTL3 is affected by its acetylation at K177. Importantly, acetylation of METTL3 blocks its interaction with EIF3H, a subunit of the translation initiation factor, thereby reducing mRNA translation efficiency. Interestingly, acetylation of METTL3 responds to oxidative stress. Mechanistically, oxidative stress enhances the interaction of PCAF with METTL3, increases METTL3 acetylation, and suppresses the interaction of METTL3 with EIF3H, thereby decreasing the translation efficiency of ribosomes and inhibiting cell proliferation. Altogether,we suggest a mechanism by which oxidative stress regulates RNA translation efficiency by the modulation of METTL3 acetylation mediated by PCAF.

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Aging hallmarks of the primate ovary revealed by spatiotemporal transcriptomics

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Protein & Cell 2024年第5期15卷 364-384页

作者： Huifen Lu Ying Jing Chen Zhang Shuai Ma Weiqi Zhang Daoyuan Huang Bin Zhang Yuesheng Zuo Yingying Qin Guang-Hui Liu Yang Yu Jing Qu Si Wang Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China State key laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Aging Translational medicine Center International Center for Aging and CancerBeijing Municipal Geriatric Medical Research CenterXuanwu HospitalCapital Medical UniversityBeijing 100053China State key laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Beijing Institute for Stem Cell and Regenerative medicine Beijing 100101China CAS key laboratory of Genomic and Precision medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China Institute for Stem cell and Regeneration CASBeijing 100101China China National Center for Bioinformation Beijing 100101China The Fifth People’s Hospital of Chongqing Chongqing 400062China Sino-Danish College University of Chinese Academy of SciencesBeijing 101408China Sino-Danish Center for Education and Research Beijing 101408China Department of Obstetrics and Gynecology Center for Reproductive MedicinePeking UniversityThird HospitalBeijing 100191China Clinical Stem Cell Research Center Peking UniversityThird HospitalBeijing 100191China Center for Reproductive medicine Cheeloo College of MedicineShandong UniversityJinan 250012China key laboratory of Reproductive Endocrinology of Ministry of Education National Research Center for Assisted Reproductive Technology and Reproductive GeneticsShandong Key Laboratory of Reproductive MedicineShandong Provincial Clinical Research Center for Reproductive HealthJinan 250012China key laboratory of Organ Regeneration and Reconstruction Institute of ZoologyChinese Academy of SciencesBeijing 100101China Aging Biomarker Consortium Beijing 100101China

The ovary is indispensable for female reproduction,and its age-dependent functional decline is the primary cause of ***,the molecular basis of ovarian aging in higher vertebrates remains poorly ***,we apply spatiotemporal transcriptomics to benchmark architecture organization as well as cellular and molecular determinants in young primate ovaries and compare these to aged primate *** a global view,somatic cells within the non-follicle region undergo more pronounced transcriptional fluctuation relative to those in the follicle region,likely constituting a hostile microenvironment that facilitates ovarian ***,we uncovered that inflammation,the senescent-associated secretory phenotype,senescence,and fibrosis are the likely primary contributors to ovarian aging(PCOA).Of note,we identified spatial co-localization between a PCOA-featured spot and an unappreciated MT2(Metallothionein 2)highly expressing spot(MT2^(high))characterized by high levels of inflammation,potentially serving as an aging hotspot in the primate ***,with advanced age,a subpopulation of MT2^(high)accumulates,likely disseminating and amplifying the senescent signal *** study establishes the first primate spatiotemporal transcriptomic atlas,advancing our understanding of mechanistic determinants underpinning primate ovarian aging and unraveling potential biomarkers and therapeutic targets for aging and age-associated human ovarian disorders.

关键词： spatial transcriptome primate ovary aging senescence inflammation

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Chinese patients with adult onset leukodystrophy caused by CST3 variants

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Journal of genetics and Genomics 2024年第7期51卷 778-780页

作者： Yi Zhang Zhi-Ying Wu Department of Medical genetics and Center for Rare Diseases Zhejiang Key Laboratory of Rare Diseases for Precision Medicine and Clinical TranslationSecond Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310009China Nanhu Brain-computer Interface Institute HangzhouZhejiang 314050China Department of Neurology Second Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310009China MOE Frontier Science Center for Brain Science and Brain-machine Integration School of Brain Science and Brain MedicineZhejiang UniversityHangzhouZhejiang 310012China

Leukodystrophies represent a group of cerebral white matter disorders that mainly affect axon-glia *** disorders are clinically diverse and display significant genetic *** is challenging to differentiate hereditary leukodystrophies,particularly those that present in adulthood,from acquired leukodystrophies and other genetic disorders,such as multiple sclerosis(MS)or hereditary spastic paraplegia(HSP)(Wei et al.,2021).Over the past few decades,a series of causative genes associated with leukodystrophies have been identified(Kohler et al.,2018).Nevertheless,a significant proportion of patients still lack a precise molecular diagnosis.

关键词： al. patients Kohler