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Recombinant adeno-associated virus 8-mediated inhibition of microRNA let-7a ameliorates sclerosing cholangitis in a clinically relevant mouse model

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World Journal of Gastroenterology 2024年第5期30卷 471-484页

作者： Hui Hua Qian-Qian Zhao Miriam Nkesichi Kalagbor Guo-Zhi Yu Man Liu Zheng-Rui Bian Bei-Bei Zhang Qian Yu Yin-Hai Xu Ren-Xian Tang Kui-Yang Zheng Chao Yan Jiangsu Key laboratory of Immunity and Metabolism Department of Pathogenic Biology and ImmunologyNational Demonstration Center for Experimental Basic Medical Science EducationLaboratory of Infection and ImmunityXuzhou Medical UniversityXuzhou 221004Jiangsu ProvinceChina Department of laboratory Medicine The Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221002Jiangsu ProvinceChina

BACKGROUND Primary sclerosing cholangitis(PSC)is characterized by chronic inflammation and it predisposes to cholangiocarcinoma due to lack of effective treatment *** adeno-associated virus(rAAV)provides a promising platform for gene therapy on such kinds of diseases.A microRNA(miRNA)let-7a has been reported to be associated with the progress of PSC but the potential therapeutic implication of inhibition of let-7a on PSC has not been *** To investigate the therapeutic effects of inhibition of a miRNA let-7a transferred by recombinant adeno-associated virus 8(rAAV8)on a xenobiotic-induced mouse model of sclerosing *** A xenobiotic-induced mouse model of sclerosing cholangitis was induced by 0.1% 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine(DDC)feeding for 2 wk or 6 wk.A single dose of rAAV8-mediated anti-let-7a-5p sponges or scramble control was injected in vivo into mice onset of DDC *** sacrifice,the liver and the serum were collected from each *** hepatobiliary injuries,hepatic inflammation and fibrosis were *** targets of let-7a-5p and downstream molecule NF-κB were detected using Western *** rAAV8-mediated anti-let-7a-5p sponges can depress the expression of let-7a-5p in mice after DDC feeding for 2 wk or 6 *** reduced expression of let-7a-5p can alleviate hepato-biliary injuries indicated by serum markers,and prevent the proliferation of cholangiocytes and biliary ***,inhibition of let-7a mediated by rAAV8 can increase the expression of potential target molecules such as suppressor of cytokine signaling 1 and Dectin1,which consequently inhibit of NF-κB-mediated hepatic *** Our study demonstrates that a rAAV8 vector designed for liver-specific inhibition of let-7a-5p can potently ameliorate symptoms in a xenobiotic-induced mouse model of sclerosing cholangitis,which provides a possible clinical translation of PSC of human.

关键词： Primary sclerosing cholangitis Recombinant adeno-associated virus 8 Let-7a-5p Therapeutic effects inflammation

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Targeting PKM2 signaling cascade with salvianic acid A normalizes tumor blood vessels to facilitate chemotherapeutic drug delivery

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Acta Pharmaceutica Sinica B 2024年第5期14卷 2077-2096页

作者： Cheng Qian Yueke Zhou Teng Zhang Guanglu Dong Mengyao Song Yu Tang Zhonghong Wei Suyun Yu Qiuhong Shen Wenxing Chen Jaesung P.Choi Juming Yan Chongjin Zhong Li Wan Jia Li Aiyun Wang Yin Lu Yang Zhao Jiangsu Key laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica Nanjing University of Chinese MedicineNanjing 210023China School of Medicine&Holistic Integrative Medicine Nanjing University of Chinese MedicineNanjing 210023China Centre for inflammation Faculty of ScienceCentenary InstituteSchool of Life SciencesUniversity of Technology SydneySydney NSW 2050Australia Jiangsu Key laboratory of Immunity and Metabolism Department of Pathogenic Biology and ImmunologyNational Experimental Demonstration Center for Basic Medicine EducationXuzhou Laboratory of Infection and ImmunityXuzhou Medical UniversityXuzhou 221004China Department of General Surgery Jiangsu Province Hospital of Chinese MedicineAffiliated Hospital of Nanjing University of Chinese MedicineNanjing 210029China Macquarie Medical School Faculty of MedicineHuman Health SciencesMacquarie UniversitySydney NSW 2109Australia

Aberrant tumor blood vessels are prone to propel the malignant progression of tumors,and targeting abnormal metabolism of tumor endothelial cells emerges as a promising option to achieve vascular normalization and antagonize tumor ***,we demonstrated that salvianic acid A(SAA)played a pivotal role in contributing to vascular normalization in the tumor-bearing mice,thereby improving delivery and effectiveness of the chemotherapeutic *** was capable of inhibiting glycolysis and strengthening endothelial junctions in the human umbilical vein endothelial cells(HUVECs)exposed to ***,SAA was inclined to directly bind to the glycolytic enzyme PKM2,leading to a dramatic decrease in endothelial *** importantly,SAA improved the endothelial integrity via activating theβ-Catenin/Claudin-5 signaling axis in a PKM2-dependent *** findings suggest that SAA may serve as a potent agent for inducing tumor vascular normalization.

关键词： Salvianic acid A Tumor vascular normalization PKM2 β-Catenin Claudin-5 Endothelial glycolysis Tight junctions Doxorubicin

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Rab18 maintains homeostasis of subcutaneous adipose tissue to prevent obesity-induced metabolic disorders

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Science China(Life Sciences) 2024年第6期67卷 1170-1182页

作者： Jiaming Liu Liangkui Li Dijin Xu Yuqi Li Tao Chen Yeyang Liu Yuqian Bao Yan Wang Longyan Yang Peng Li Li Xu State Key laboratory of Membrane biology and Tsinghua-Peking Center for Life Sciences Beijing Advanced Innovation Center for Structural BiologySchool of Life SciencesTsinghua UniversityBeijing 100084China Shanghai Qi Zhi Institute Shanghai 200232China Shanghai Key laboratory of Metabolic Remodeling and Health Institute of Metabolism and Integrative BiologyFudan UniversityShanghai 200438China Tianjian laboratory of Advanced Biomedical Sciences Zhengzhou UniversityZhengzhou 450001China Department of Physiology School of Basic Medical SciencesGannan Medical UniversityGanzhou 341000China Department of Endocrinology and Metabolism Shanghai Jiao Tong University School of Medicine Affiliated Sixth People’s HospitalShanghai 200025China Center for Endocrine Metabolism and Immune Diseases Beijing Luhe HospitalCapital Medical UniversityBeijing 101149China Beijing Key laboratory of Diabetes Research and Care Beijing 101149China

Metabolically healthy obesity refers to obese individuals who do not develop metabolic *** people store fat in subcutaneous adipose tissue(SAT)rather than in visceral adipose tissue(VAT).However,the molecules participating in this specific scenario remain ***18,a lipid droplet(LD)-associated protein,mediates the contact between the endoplasmic reticulum(ER)and LDs to facilitate LD growth and *** the present study,we show that the protein level of Rab18 is specifically upregulated in the SAT of obese people and ***18 adipocyte-specific knockout(Rab18 AKO)mice had a decreased volume ratio of SAT to VAT compared with wildtype *** subjected to high-fat diet(HFD),Rab18 AKO mice had increased ER stress and inflammation,reduced adiponectin,and decreased triacylglycerol(TAG)accumulation in *** contrast,TAG accumulation in VAT,brown adipose tissue(BAT)or liver of Rab18AKO mice had a moderate increase without ER stress ***18 AKO mice developed insulin resistance and systematic ***18 AKO mice maintained body temperature in response to acute and chronic cold induction with a thermogenic SAT,similar to the counterpart ***,Rab18-deficient 3T3-L1 adipocytes were more prone to palmitate-induced ER stress,indicating the involvement of Rab18 in alleviating lipid ***18 AKO mice provide a good animal model to investigate metabolic disorders such as impaired *** conclusion,our studies reveal that Rab18 is a key and specific regulator that maintains the proper functions of SAT by alleviating lipid-induced ER stress.

关键词： Rab18 subcutaneous adipose tissue(SAT) metabolically healthy obesity(MHO) lipotoxicity ER stress ectopic lipid storage LD-ER contact

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Targeting a disintegrin and metalloprotease(ADAM)17-CD122 axis enhances CD8^(+)T cell effector differentiation and anti-tumor immunity

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Signal Transduction and Targeted Therapy 2024年第7期9卷 3097-3111页

作者： Lina Sun Anjun Jiao Haiyan Liu Renyi Ding Ning Yuan Biao Yang Cangang Zhang Xiaoxuan Jia Gang Wang Yanhong Su Dan Zhang Lin Shi Chenming Sun Aijun Zhang Lianjun Zhang Baojun Zhang Department of Pathogenic Microbiology and Immunology School of Basic Medical SciencesXi’an Jiaotong UniversityXi’anShaanxi 710061China Institute of infection and Immunity Translational Medicine InstituteXi’an Jiaotong University Health Science CenterXi’anShaanxi 710061China Key laboratory of Environment and Genes Related to Diseases Ministry of EducationXi’anShaanxi 710061China Xi’an Key laboratory of Immune Related Diseases Xi’anShannxi 710061China Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy Cancer InstituteXuzhou Medical UniversityXuzhouJiangsuChina Department of Pediatrics Qilu Hospital of Shandong UniversityJinanChina National Key laboratory of Immunity and inflammation Suzhou Institute of Systems MedicineChinese Academy of Medical Sciences&Peking Union Medical CollegeSuzhou 215123 JiangsuChina Key laboratory of Synthetic biology Regulatory Elements Suzhou Institute of Systems MedicineChinese Academy of Medical Sciences&Peking Union Medical CollegeSuzhou 215123 JiangsuChina

CD8^(+)T cell immune responses are regulated by multi-layer networks,while the post-translational regulation remains largely *** ectodomain shedding is an important post-translational process orchestrating receptor expression and signal transduction through proteolytic cleavage of membrane ***,by targeting the sheddase A Disintegrin and Metalloprotease(ADAM)17,we defined a post-translational regulatory mechanism mediated by the ectodomain shedding in CD8^(+)T *** and proteomic analysis revealed the involvement of post-translational regulation in CD8^(+)T cells.T cellspecific deletion of ADAM17 led to a dramatic increase in effector CD8^(+)T cell differentiation and enhanced cytolytic effects to eliminate pathogens and ***,ADAM17 regulated CD8^(+)T cells through cleavage of membrane ***17 inhibition led to elevated CD122 expression and enhanced response to IL-2 and IL-15 stimulation in both mouse and human CD8^(+)T ***,inhibition of ADAM17 in CD8^(+)T cells improved the efficacy of chimeric antigen receptor(CAR)T cells in solid *** findings reveal a critical post-translational regulation in CD8^(+)T cells,providing a potential therapeutic strategy of targeting ADAM17 for effective anti-tumor immunity.

关键词： immunity stimulation involvement

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A novel structural variant of RET causes familial Hirschsprung's disease via nonsense-mediated mRNA decay

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Genes & Diseases 2024年第1期11卷 7-10页

作者： Qi Wang Siyu Pu Bo Xiang Jing Chen Department of Pediatric Surgery and laboratory of Pediatric Surgery Rare Diseases CenterInstitute of Immunology and InflammationFrontiers Science Center for Disease-Related Molecular NetworkWest China HospitalSichuan UniversityChengduSichuan 610041China

Hirschsprung's disease(HsCR)is the most common type of developmental gastrointestinal malformation causing intestinal obstruction in children,with an incidence of 1/5000 in live births.1 it is characterized by the absence of intrinsic ganglion cells in the myenteric and submucosal plexuses of the distal gastrointestinal tract,leading to the dysregulation of smooth muscle contraction/relaxation and resulting in intestinal *** on the length of the aganglionic intestine,HSCR can be categorized into short-segmental HSCR(S-HSCR),which affects up to the sigmoid colon from the anus,and long-segmental HSCR(LHSCR),which affects beyond the sigmoid colon.1 In some rare conditions,aganglionic lesions can affect the full length of the colon or even the whole intestine.

关键词： intestine colon relaxation

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Reduced clinical severity during 2022 Shanghai Spring epidemic of SARS-CoV-2 omicron BA.2 variant infection——an integrated account of virus pathogenicity and vaccination effectiveness

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National Science Review 2024年第4期11卷 24-27页

作者： Xingyue Wu Yao Chen Kangli Cao Yao Shen Xueling Wu Yilin Yang Zhongshu Kuang Qingrun Li Zhenzhen Lu Yichen Jia Mian Shao Guorong Gu Xiangwei Wang Ye Yao Ying Wang Shaodie Chen Zhigao Yu Wei Wei Longfei Ding Lulu Lan Tianwen Gu Xiangyu Long Jian Sun Lingyu Xing Jiayuan Shen Yi Han Yue Luo Sucheng Mu Mengna Lin Xiaoyan Zhang Rong Zeng Jianqing Xu Guoping Zhao Lihong Huang Zhenju Song Department of Emergency Medicine Clinical Center for Bio-Therapy Department of Biostatistics and Department of UrologyShanghai Key Laboratory of Lung Inflammation and Injury Zhongshan Hospital Fudan University Department of Respiratory and Critical Care Medicine Shanghai Pudong Hospital Fudan University Department of Pulmonology Renji Hospital Shanghai Jiao Tong University School of Medicine Key laboratory of Systems biology Center for Excellence in Molecular Cell Science Shanghai Institute of Biochemistry and Cell Biology Chinese Academy of Sciences Shanghai Public Health Clinical Center Fudan University Department of Biostatistics School of Public Health Key Laboratory of Public Health Safety of Ministry of Education and Shanghai Institute of Infectious Disease and Biosecurity School of Public Health Fudan University Shanghai Institute of Immunology Department of Immunology and Microbiology Shanghai Institute of Virology Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of EducationSchool of Medicine Shanghai Jiao Tong University State Key laboratory of Genetic Engineering Fudan Microbiome CenterSchool of Life Sciences Fudan University Bio-Med Big Data Center Shanghai Institute of Nutrition and Health Chinese Academy of Sciences

The emergence of SARS-Co V-2 variant of concern omicron BA.2 led to high infection incidence rates as well as reduced severity of COVID-19 during the Shanghai Spring epidemic of 2022 [1]. We assessed the role of viral pathogenicity and the effectiveness of inactivated vaccines in a retrospective observational study including 10 258 confirmed COVID-19cases identified between April and June of 2022, from four COVID-19 designated hospitals located in two areas of Shanghai, namely the West Bund and the East Bund, where the populations’ demographic characteristics varied significantly (Table S1, Fig. S1).

关键词： REPLICATION

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An antibiotic-free platform for eliminating persistent Helicobacter pylori infection without disrupting gut microbiota

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Acta Pharmaceutica Sinica B 2024年第7期14卷 3184-3204页

作者： Yongkang Lai Tinglin Zhang Xiaojing Yin Chunping Zhu Yiqi Du Zhaoshen Li Jie Gao Department of Gastroenterology Shanghai Changhai HospitalNaval Medical UniversityShanghai 200433China Changhai Clinical Research Unit Shanghai Changhai HospitalNaval Medical UniversityShanghai 200433China Department of Gastroenterology Ganzhou People’s Hospital Affiliated to Nanchang UniversityGanzhou 341000China National Key laboratory of Immunity and inflammation Naval Medical UniversityShanghai 200433China Shanghai Key laboratory of Nautical Medicine and Translation of Drugs and Medical Devices Shanghai 200433China

Helicobacter pylori(***)infection remains the leading cause of gastric adenocarcinoma,and its eradication primarily relies on the prolonged and intensive use of two ***,antibiotic resistance has become a compelling health issue,leading to *** eradication treatment failure ***,the powerlessness of antibiotics against biofilms,as well as intracellular *** and the long-term damage of antibiotics to the intestinal microbiota,have also created an urgent demand for antibiotic-free ***,we describe an antibiotic-free,multifunctional copperorganic framework(HKUST-1)platform encased in a lipid layer comprising phosphatidic acid(PA),rhamnolipid(RHL),and cholesterol(CHOL),enveloped in chitosan(CS),and loaded in an ascorbyl palmitate(AP)hydrogel:AP@CS@Lip@*** platform targets inflammatory sites where *** aggregates through electrostatic ***,hydrolysis by matrix metalloproteinases(MMPs)releases CS-encased nanoparticles,disrupting bacterial urease activity and membrane ***,RHL disperses biofilms,while PA promotes lysosomal acidification and activates host autophagy,enabling clearance of intracellular ***,AP@CS@Lip@HKUST-1 alleviates inflammation and enhances mucosal repair through delayed Cu^(2+) release while preserving the intestinal ***,this platform presents an advanced therapeutic strategy for eradicating persistent *** infection without inducing drug resistance.

关键词： Helicobacter pylori infection Antibiotic-free Biofilms Autophagy Gastric mucosal repair Drug resistance Intestinal microbiota Anti-inflammation

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Identification of a natural PLA2 inhibitor from the marine fungus Aspergillus sp.c1 for MAFLD treatment that suppressed lipotoxicity by inhibiting the IRE-1a/XBP-1s axis and JNK signaling

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Acta Pharmaceutica Sinica B 2024年第1期14卷 304-318页

作者： Yong Rao Rui Su Chenyan Wu Xingxing Chai Jinjian Li Guanyu Yang Junjie Wu Tingting Fu Zhongping Jiang Zhikai Guo Congjun Xu Ling Huang Key laboratory of Tropical Biological Resources of Ministry of Education School of Pharmaceutical SciencesHainan UniversityHaikou 570200China Hainan Key laboratory of Tropical Microbe Resources Institute of Tropical Bioscience and BiotechnologyChinese Academy of Tropical Agricultural Sciences&Key Laboratory for Biology and Genetic Resources of Tropical Crops of Hainan ProvinceHainan Institute for Tropical Agricultural ResourcesHaikou 571101China School of Pharmaceutical Sciences Guangdong Provincial Key Laboratory of New Drug Design and EvaluationSun Yat-sen UniversityGuangzhou 510275China laboratory Animal Center of Guangdong Medical University Dongguan 523808China

Lipotoxicity is a pivotal factor that initiates and exacerbates liver injury and is involved in the development of metabolic-associated fatty liver disease(MAFLD).However,there are few reported lipotoxicity ***,we identified a natural anti-lipotoxicity candidate,HN-001,from the marine fungus Aspergillus ***-001 dose-and time-dependently reversed palmitic acid(PA)-induced hepatocyte *** protection was associated with IRE-1a-mediated XBP-1 splicing inhibition,which resulted in suppression of XBP-1s nuclear translocation and transcriptional *** of XBP-1s attenuated lipotoxicity,but no additional ameliorative effect of HN-001 on lipotoxicity was observed in XBP-1s knockdown ***,the ER stress and lipotoxicity amelioration was associated with *** HN-001 and the PLA2 inhibitor MAFP inhibited PLA2 activity,reduced lysophosphatidylcholine(LPC)level,subsequently ameliorated *** contrast,overexpression of PLA2 caused exacerbation of lipotoxicity and weakened the anti-lipotoxic effects of ***,HN-001 treatment suppressed the downstream pro-apoptotic JNK *** vivo,chronic administration of HN-001(i.p.)in mice alleviated all manifestations of MAFLD,including hepatic steatosis,liver injury,inflammation,and *** effects were correlated with PLA2/IRE-1a/XBP-1s axis and JNK signaling *** data indicate that HN-001 has therapeutic potential for MAFLD because it suppresses lipotoxicity,and provide a natural structural basis for developing anti-MAFLD candidates.

关键词： Lipotoxicity MAFLD ER stress IRE-1a XBP-1s JNK PLA2

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Ultrasmall copper-based clusterzymes ameliorate Achilles tendinopathy by inhibiting acute oxidative stress

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Nano Research 2024年第6期17卷 5374-5389页

作者： Xuzhuo Chen Yi Du Yazi Huang Xianhao Zhou Xinru Xie Chang Li Chen Zhao Fengrong Dai Xijiao Yu Shanyong Zhang Department of Oral Surgery Shanghai Ninth People’s HospitalShanghai Jiao Tong University School of MedicineCollege of StomatologyShanghai Jiao Tong UniversityNational Center for StomatologyNational Clinical Research Center for Oral DiseasesShanghai Key Laboratory of StomatologyShanghai Research Institute of StomatologyShanghai 200011China Department of Endodontics Central LaboratoryJinan Stomatological HospitalJinan Key Laboratory of Oral Tissue RegenerationShandong Provincial Health Commission Key Laboratory of Oral Diseases and Tissue RegenerationJinan 250001China State Key laboratory of structural Chemistry Fujian Institute of Research on the Structure of MatterChinese Academy of SciencesFuzhou 350002China Department of Chemistry College of Chemistry and EnvironmentGuangdong Ocean UniversityZhanjiang 524088China Department of Orthopedics Shanghai Key Laboratory of Orthopedic ImplantShanghai Ninth People's HospitalShanghai Jiao Tong University School of MedicineShanghai 200011China

Tendinopathy is a prevalent musculoskeletal disorder,accounting for over 30%of musculoskeletal ***,current therapeutic strategies for tendinopathy are limited and often yield unsatisfactory clinical ***,there is a critical need to explore novel therapeutic approaches with minimal side effects for tendinopathy and its early *** this study,we successfully designed and synthesized a copper(I)-based nanocluster,named Cu_(11),which possesses remarkable enzyme-like and ROS-scavenging *** unique combination of properties qualifies Cu_(11)as an attractive anti-inflammatory and anti-ROS *** Cu_(11)clusterzymes specifically target mitochondria,effectively scavenging excessive reactive oxygen species(ROS)and reducing oxidative ***,Cu_(11)clusterzymes inhibit the activation of key signaling pathways involved in inflammation,namely tumor necrosis factor(TNF),mitogen-activated protein kinase(MAPK),and nuclear factor(NF)-κB,leading to a decrease in the release of proinflammatory ***,our in vivo experiments using a collagenase-induced acute Achilles tendinopathy model demonstrated that Cu_(11)clusterzymes effectively alleviate inflammation and oxidative stress,without causing systemic *** study highlights the potential of copper-based clusterzymes as therapeutic agents for the treatment of Achilles tendinopathy and other inflammatory *** unique enzyme-like and ROS-scavenging activities of Cu_(11)make it a promising candidate for further development and clinical translation.

关键词： nanoclusters clusterzymes oxidative stress tendinopathy reactive oxygen species(ROS)

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Liberation of SARS-CoV main protease from the viral polyprotein:N-terminal autocleavage does not depend on the mature dimerization mode

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Protein & Cell 2010年第3期1卷 59-74页

作者： Shuai Chen Felix Jonas Can Shen Rolf Higenfeld Institute of Biochemistry Center for Structural and Cell Biology in MedicineUniversity of LübeckRatzeburger Allee 16023538 LübeckGermany laboratory for structural biology of infection and inflammation c/o DESYBuilding 22aNotkestr.8522603 HamburgGermany

The main protease(M^(pro))plays a vital role in proteolytic processing of the polyproteins in the replicative cycle of SARS coronavirus(SARS-CoV).Dimerization of this enzyme has been shown to be indispensable for transcleavage ***,the auto-processing mechanism of M^(pro),*** own release from the polyproteins through autocleavage,remains *** study elucidates the relationship between the N-terminal autocleavage activity and the dimerization of“immature”M^(pro).Three residues(Arg4,Glu290,and Arg298),which contribute to the active dimer conformation of mature M^(pro),are selected for mutational ***,all three mutants still perform N-terminal autocleavage,while the dimerization of mature protease and transcleavage activity following auto-processing are completely inhibited by the E290R and R298E mutations and partially so by the R4E ***,the mature E290R mutant can resume N-terminal autocleavage activity when mixed with the“immature”C145A/E290R double mutant whereas its trans-cleavage activity remains ***,the N-terminal auto-processing of M^(pro) appears to require only two“immature”monomers approaching one another to form an“intermediate”dimer structure and does not strictly depend on the active dimer conformation existing in mature *** conclusion,an auto-release model of M^(pro) from the polyproteins is proposed,which will help understand the auto-processing mechanism and the difference between the autocleavage and trans-cleavage proteolytic activities of SARS-CoV M^(pro).

关键词： SARS-CoV M^(pro) N-terminal autocleavage autocleavage activity trans-cleavage activity dimerization

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