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Inhibition of METTL3 in macrophages provides protection against intestinal inflammation

Cellular & Molecular Immunology 2024年第6期21卷 589-603页

作者： Huilong Yin Zhuan Ju Xiang Zhang Wenjie Zuo Yuhang Yang Minhua Zheng Xiaofang Zhang Yuning Liu Yingran Peng Ying Xing Angang Yang Rui Zhang Henan Key Laboratory of Immunology and Targeted Therapy School of Medical TechnologyXinxiang Medical UniversityXinxiangHenan453003China Molecular Immunology and Immunotherapy Laboratory School of Medical TechnologyXinxiang Medical UniversityXinxiangHenan453003China Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine School of Medical TechnologyXinxiang Medical UniversityXinxiangHenan453003China State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Department of Immunology Fourth Military Medical UniversityXi’anShaanxi710032China State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Department of Biochemistry and Molecular Biology Fourth Military Medical UniversityXi’anShaanxi710032China State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Department of Medical Genetics and Developmental Biology Fourth Military Medical UniversityXi’anShaanxi710032China Department of Endocrinology Xi’an Daxing HospitalXi’anShaanxi710000China

Inflammatory bowel disease(IBD)is prevalent,and no satisfactory therapeutic options are available because the mechanisms underlying its development are poorly *** this study,we discovered that increased expression of methyltransferase-like 3(METTL3)in macrophages was correlated with the development of colitis and that depletion of METTL3 in macrophages protected mice against dextran sodium sulfate(DSS)-induced *** characterization indicated that METTL3 depletion increased the YTHDF3-mediated expression of phosphoglycolate phosphatase(PGP),which resulted in glucose metabolism reprogramming and the suppression of CD4+T helper 1(Th1)cell *** analysis revealed that glucose metabolism contributed to the ability of METTL3 depletion to ameliorate colitis *** addition,we developed two potent small molecule METTL3 inhibitors,namely,F039-0002 and 7460-0250,that strongly ameliorated DSS-induced ***,our study suggests that METTL3 plays crucial roles in the progression of colitis and highlights the potential of targeting METTL3 to attenuate intestinal inflammation for the treatment of colitis.

关键词： Colitis Glucose metabolism Macrophage n6-methyladenosine modification

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nanodrug enhances post-ablation immunotherapy of hepatocellular carcinoma via promoting dendritic cell maturation and antigen presentation

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Bioactive Materials 2023年第3期21卷 57-68页

作者： Zecong Xiao Tan Li Xinyao Zheng Liteng Lin Xiaobin Wang Bo Li Jingjun Huang Yong Wang Xintao Shuai Kangshun Zhu Department of Minimally Invasive Interventional Radiology And Laboratory of Interventional RadiologyThe Second Affiliated Hospital of Guangzhou Medical UniversityGuangzhou510260China nanomedicine Research Center The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhou510630China College of Chemistry and Materials Science Jinan UniversityGuangzhou510632China Department of Dermatology The Nanfang Hospital of Southern Medical UniversityGuangzhouGuangdong510515China

Thermal ablation(TA)as an effective method treating hepatocellular carcinoma(HCC)in clinics is facing great challenges of high recurrence and *** immune-checkpoint blockade(ICB)-based immuno-therapy has shown potential to inhibit recurrence and metastasis,the combination strategy of ICB and thermal ablation has shown little progress in HCC *** tremendous hurdle for combining ICB with thermal ablation lies with the insufficient antigen internalization and immaturity of tumor-infiltrating dendritic cells(TIDCs)which leads to an inferior immune response to distant tumor growth and ***,an antigen-capturing nanoplatform,whose surface was modified with mannose as a targeting ligand,was constructed for co-delivering tumor-associated antigens(TAAs)and m6A demethylases inhibitor(i.e.,fat mass and obesity asso-ciated gene(FTO)inhibitor)into *** vivo results demonstrate that the intratumoral injection of nanodrug followed by HCC thermal ablation promotes dendritic cells(DCs)maturation,improves tumor infiltration of effector T cells and generates immune memory,which synergize with ICB treatment to inhibit the distant tumor growth and lung ***,the antigen-capturing and FTO-inhibiting nanodrug holds potential to boost the ICB-based immunotherapy against HCC after thermal ablation.

关键词： Thermal ablation Tumor-infiltrating dendritic cells n6-methyladenosine modification nanoplatform Tumor immunotherapy

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The Genetic Association between CDKn1A and Heart Failure:Genome-Wide Exploration of m6A-SnPs and Mendelian Randomization

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Biomedical and Environmental Sciences 2024年第12期37卷 1397-1408页

作者： Ziyi Yang Zhennan Lin Xiaotong ning Xingbo Mo Laiyuan Wang Xiangfeng Lu Shufeng Chen Key Laboratory of Cardiovascular Epidemiology Department of EpidemiologyFuwai HospitalNational Center for Cardiovascular DiseasesChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100037China Center for Genetic Epidemiology and Genomics Department of EpidemiologyJiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric DiseasesSchool of Public HealthMedical College of Soochow UniversitySuzhou 215123JiangsuChina

Objective n6-methyladenosine(m^(6)A)is a common epigenetic modification in *** this study,we explore the potential impact of m^(6)A-associated single nucleotide polymorphisms(m^(6)A-SnPs)on heart failure(HF).Methods Data from genome-wide association studies(GWAS)investigating HF in humans and from m^(6)A-SnPs datasets were used to identify HF-associated m^(6)*** functions were explored using expression quantitative trait locus(eQTL),gene expression,and gene enrichment *** protein quantitative trait locus(pQTL)-Mendelian randomization(MR)was used to investigate the potential mechanism between critical protein levels and risk factors for *** We screened 44 HF-associated m^(6)A-SnPs,including 10 m^(6)A-SnPs that showed eQTL signals and differential expressions in *** SnP rs1801270 in CDKn1A showed the strongest association with HF(P=7.75×10^(−6)).Additionally,MR verified the genetic association between the CDKn1A protein and HF,as well as the mediating effect of blood pressure(BP)in this *** circulating level of CDKn1A was associated with a lower risk of HF(odds ratio[OR]=0.82,95%confidence interval[CI]:0.69 to 0.99).The proportions of hypertension,systolic BP,and diastolic BP were 48.10%,28.94%,and 18.02%,*** of PDIA6(P=1.30×10^(−2))and SMAD3(P=4.80×10^(−2))with HF were also *** Multiple HF-related m^(6)A-SnPs were identified in this *** associations of CDKn1A and other proteins with HF and its risk factors were demonstrated,providing new ideas for further exploration of the molecular mechanisms of HF.

关键词： Heart failure n6-methyladenosine modification Genome-wide association study Expression quantitative trait locus Mendelian randomization

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