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Hepatocellular SETDB1 Regulates Hepatic Ischemia-Reperfusion Injury through Targeting Lysine Methylation of ASK1 Signal

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Research 2024年第3期6卷 305-317页

作者： Kang Xia Tianyu Wang Zhongbao Chen Jiayu Guo Bo Yu Qi Chen Tao Qiu Jiangqiao Zhou Shusen Zheng Department of organ transplantation Renmin Hospital of Wuhan UniversityWuhanChina Department of Urology Renmin Hospital of Wuhan UniversityWuhanChina. Department of general surgery Renmin Hospital of Wuhan UniversityWuhanChina Division of Hepatobiliary and Pancreatic Surgery Department of SurgeryFirst Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhouChina key laboratory of {2. multi-organ transplantation Ministry of Public HealthHangzhouChina key laboratory of {2. transplantation HangzhouZhejiang ProvinceChina key laboratory of the Diagnosis and Treatment of {2. transplantation CAMSHangzhouChina.

Background: Hepatic ischemia-reperfusion injury (HIRI) stands as an unavoidable complication arising from liver surgery, profoundly intertwined with its prognosis. The role of lysine methyltransferase SET domain bifurcated 1 (SETDB1) in HIRI remains elusive, despite its confirmation as a potential therapeutic target for diverse diseases. Here, we investigated the mechanism by which SETDB1 regulated HIRI. Methods: RNA sequencing data were used to identify the expression and potential targets of SETDB1 through bioinformatics analysis. To elucidate the impact of SETDB1 on HIRI, both an in vivo model of HIRI in mice and an in vitro model of hepatocyte hypoxia/reoxygenation were established. Biochemical and histological analyses were used to investigate the influence of SETDB1 on liver damage mediated by HIRI. Chromatin immunoprecipitation and coimmunoprecipitation were implemented to explore the in-depth mechanism of SETDB1 regulating HIRI. Results: We confirmed that hepatocellular SETDB1 was up-regulated during HIRI and had a close correlation with HIRI-related inflammation and apoptosis. Moreover, inhibition of SETDB1 could mitigate HIRI-induced liver damage, inflammation, and apoptosis. Through our comprehensive mechanistic investigation, we revealed that SETDB1 interacts with apoptosis-signal-regulating kinase 1 (ASK1) and facilitates the methylation of its lysine residues. Inhibition of SETDB1 resulted in reduced phosphorylation of ASK1, leading to a marked suppression of downstream c-Jun N-terminal kinase (JNK)/p38 signaling pathway activation. The therapeutic effect on inflammation and apoptosis achieved through SETDB1 inhibition was nullified by the restoration of JNK/p38 signaling activation through ASK1 overexpression. Conclusions: The findings from our study indicate that SETDB1 mediates lysine methylation of ASK1 and modulates the activation of the ASK1–JNK/p38 pathway, thus involved in HIRI-induced inflammation and apoptosis. These results suggest that SETD

关键词： SETDB1 inflammation ASK1

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Addressing chemoresistance with a lipid gemcitabine nanotherapeutic strategy for effective treatment of pancreatic cancer

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Nano Research 2024年第9期17卷 8377-8388页

作者： Jiawei Hong Shiyun Xian Shusen Zheng Hangxiang Wang Donghai Jiang The First Affiliated Hospital NHC Key Laboratory of Combined Multi-Organ TransplantationCollaborative Innovation Center for Diagnosis and Treatment of Infectious DiseasesState Key Laboratory for Diagnosis and Treatment of Infectious DiseasesSchool of MedicineZhejiang UniversityHangzhou 310003China Jinan Microecological Biomedicine Shandong laboratory Jinan 250117China

Resistance to gemcitabine in pancreatic cancer poses a significant clinical *** investigation is warranted to assess whether nano-formulation strategy can be employed to enhance the sensitivity of resistant strains to gemcitabine *** this study,using gemcitabine-resistant pancreatic cancer cell lines,we examined the therapeutic potential of a gemcitabine nanodelivery platform and assessed the ability to overcome drug resistance against resistant *** of human equilibrative nucleoside transporter 1(hENT1)led to reduced cellular uptake of gemcitabine,resulting in chemoresistance in pancreatic *** nanoparticles circumvented the entry blockade caused by hENT1 silencing through *** entry via clathrin-mediated endocytosis increased intracellular gemcitabine accumulation in gemcitabine-resistant pancreatic cancer ***,gemcitabine nanoparticles are preferential in vivo delivery to tumor tissues,likely due to the enhanced permeability and retention *** comparison to free gemcitabine,gemcitabine nanoparticles demonstrate a more pronounced cytotoxic effect on gemcitabine-resistant pancreatic cancer cells,with favorable *** study improved the efficacy of gemcitabine through nanotechnology,providing a novel strategy to address gemcitabine-resistant pancreatic cancer.

关键词： pancreatic cancer gemcitabine resistance gemcitabine nanoparticle human equilibrative nucleoside transporter 1

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M2.type macrophage membrane-mediated delivery of Carvedilol nanocomplex for acute liver failure treatment and remodeling inflammatory microenvironment

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Nano Research 2024年第7期17卷 6362-6375页

作者： Mingge Shang Yaohui Zhang Junjie Qian Wenchao Wang Xizhi Yu Jiacheng Huang Lin Zhou Shusen Zheng Division of Hepatobiliary and Pancreatic Surgery Department of SurgeryThe First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China NHC key laboratory of {2. multi-organ transplantation Key Laboratory of Organ TransplantationHangzhou 310003China key laboratory of the diagnosis and treatment of {2. transplantation Research Unit of Collaborative Diagnosis and Treatment for Hepatobiliary and Pancreatic CancerChinese Academy of Medical Sciences(2019RU019)Hangzhou 310003China State key laboratory for Diagnosis and Treatment of Infectious Diseases National Clinical Research Center for Infectious DiseasesHangzhou 310003China Department of Thyroid Surgery The First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China Shulan(Hangzhou)Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College Hangzhou 310000China

Interactions of hepatic macrophages with local inflammatory microenvironment is the key factor promoting the development of acute liver failure(ALF).Hence,reprogramming pro-inflammatory M1 into anti-inflammatory M2.phenotype may offer a promising strategy for treating ALF by targeting *** group found Carvedilol possessed potential anti-inflammatory property previously,which had been scarcely reported in *** present a synergy strategy to induce macrophages into the phenotype M2.type anti-inflammatory macrophages with interleukin-4(IL-4)and IL-10 at *** Carvedilol is loaded on the macrophage membrane-camouflaged biomimetic nano-platform(termed as M2.@CNP)to evade reticuloendothelial system(RES)and afford Carvedilol delivery to the inflammatory environment with overproduced reactive oxygen species(ROS),further prolonging its circulation and *** released Carvedilol produced anti-inflammatory,antioxidant and anti-apoptosis effects,combining local M2.type cell membranes(M2.CM)inhibited pro-inflammatory cytokines and ROS levels,which in turn promoted and amplified M1 to M2.phenotype polarization *** study offers new insights into the rational design of biomimetic nanosystems for safe and effective ALF therapy to accelerate the clinical translation.

关键词： acute liver failure hepatic drug delivery M2.macrophage-camouflaged nanoplatform inflammatory microenvironment macrophage polarization

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Polyaspers A and B,the First Ergosterol-Polyether Adducts with Unprecedented 6/6/6/5/5/6/6/6/6 Nonacyclic Architecture from Aspergillus ***507

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Chinese Journal of Chemistry 2024年第7期42卷 743-751页

作者： Hong Hu Lanqin Li Zhengyi Shi Xueqi Lan Yeting Zhang Xinye Huang Xincai Hao Qun Zhou Weiguang Sun Changxing Qi Yonghui Zhang Hubei key laboratory of Natural Medicinal Chemistry and Resource Evaluation Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China Institute of organ transplantation Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Key Laboratory of Organ TransplantationMinistry of EducationNHC Key Laboratory of Organ TransplantationKey Laboratory of Organ TransplantationChinese Academy of Medical SciencesWuhanHubei 430030China Hubei key laboratory of Wudang Local Chinese Medicine Research Hubei Engineering Technology Center for Comprehensive Utilization of Medicinal PlantsCollege of PharmacyHubei University of MedicineShiyanHubei 442000China

Psoriasis is a chronic immune-mediated inflammatory skin disease and the TNF-αis an important therapeutic target of this *** our continuous study of bioactive natural products from fungi,the first ergosterol-polyether adducts,polyaspers A(1)and B(2.,along with two known ergosterols,(36,5α,6α,2.E)-5,6-epoxy-3-hydroxyergosta-8,2.-dien-7-one(3)and calvasterol B(4),were iso-lated from Aspergillus *** elucidation was accomplished by extensive spectroscopic analysis and single-crystal X-ray diffraction *** A and B possessing an unequalled 6/6/6/5/5/6/6/6/6 nonacyclic system,and their biosynthetic path-ways were proposed to include intermolecular cyclization and Diels-Alder *** screen of these isolates showed that 1-3 could improve the cell viability in an actinomycin D/TNF-αinduced L92. cells death model,with the EC50 values of 49.85,46.75 and 4.99μmol/L,respectively,and the activity of 3 was even comparable with that of the positive control *** bioactive investigations discovered 3 could suppress the inflammatory response simulated with TNF-αin HaCaT *** an imiquimod-induced psoriasis murine model,3 significantly restrained the development of psoriasis symptoms and reduced the expression of IL-17 and IL-2.,presenting an anti-psoriatic *** such,those ergosterol derivatives,might serve as lead compounds for the development of novel TNF-αinhibitory agents in the clinical treatment of psoriasis.

关键词： Psoriasis Aspergillus sp.TJ507 TNF-α Ergosterol-polyether adducts Inflammatory skin disease

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Integrative analysis of the transcriptome and metabolome reveals the importance of hepatokine FGF2. in liver aging

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Genes & Diseases 2024年第5期11卷 407-427页

作者： Wenchao Wang Junjie Qian Mingge Shang Yiting Qiao Jiacheng Huang Xinxin Gao Zhou Ye Xinyu Tong Kangdi Xu Xiang Li Zhengtao Liu Lin Zhou Shusen Zheng Division of Hepatobiliary and Pancreatic Surgery Department of SurgeryFirst Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhouZhejiang 310003China NHC key laboratory of {2. multi-organ transplantation HangzhouZhejiang 310003China key laboratory of the Diagnosis and Treatment of {2. transplantation Research Unit of Collaborative Diagnosis and Treatment for Hepatobiliary and Pancreatic CancerChinese Academy of Medical Sciences(2019RU019)HangzhouZhejiang 310003China key laboratory of {2. transplantation Research Center for Diagnosis and Treatment of Hepatobiliary DiseasesHangzhouZhejiang 310003China Shulan International Medical College Zhejiang Shuren UniversityHangzhouZhejiang 310015China Shulan(Hangzhou)Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College HangzhouZhejiang 310000China

Aging is a contributor to liver ***,the concept of liver aging has become prominent and has attracted considerable interest,but its underlying mechanism remains poorly *** our study,the internal mechanism of liver aging was explored via multi-omics analysis and molecular experiments to support future targeted *** aged rat liver model was established with D-galactose,and two other senescent hepatocyte models were established by treating HepG2.cells with D-galactose and *** then performed transcriptomic and metabolomic assays of the aged liver model and transcriptome analyses of the senescent hepatocyte *** livers,genes related to peroxisomes,fatty acid elongation,and fatty acid degradation exhibited down-regulated expression with aging,and the hepatokine Fgf2. expression was positively correlated with the down-regulation of these *** senescent hepatocytes,similar to the results found in aged livers,FGF2. expression was also ***,the expressions of cell cycle-related genes were significantly down-regulated,and the down-regulated gene E2.8 was the key cell cycle-regulating transcription *** then validated that FGF2. overexpression can protect against liver aging and that FGF2. can attenuate the declines in the antioxidant and regenerative capacities in the aging *** successfully validated the results from cellular and animal experiments using human liver and blood *** study indicated that FGF2. is an important target for inhibiting liver aging and suggested that pharmacological prevention of the reduction in FGF2. expression due to aging may be used to treat liver aging-related diseases.

关键词： Antioxidant capability FGF2. Liver aging Liver regeneration multiomics analysis

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SERPINE2.promotes liver cancer metastasis by inhibiting c-Cbl-mediated EGFR ubiquitination and degradation

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Cancer Communications 2024年第3期44卷 384-407页

作者： Shiyu Zhang Xing Jia Haojiang Dai Xingxin Zhu Wenfeng Song Suchen Bian Hao Wu Shinuo Chen Yangbo Tang Junran Chen Cheng Jin Mengqiao Zhou Haiyang Xie Shusen Zheng Penghong Song Division of Hepatobiliary and Pancreatic Surgery Department of SurgeryThe First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiangP.R.China National Health Commission key laboratory of {2. multi-organ transplantation HangzhouZhejiangP.R.China key laboratory of the Diagnosis and Treatment of {2. transplantation Research Unit of Collaborative Diagnosis and Treatment for Hepatobiliary and Pancreatic CancerChinese Academy of Medical SciencesHangzhouZhejiangP.R.China key laboratory of {2. transplantation Research Center for Diagnosis and Treatment of Hepatobiliary DiseasesHangzhouZhejiangP.R.China State key laboratory for Diagnosis and Treatment of Infectious Diseases First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiangP.R.China

Background:Liver cancer is a malignancy with high morbidity and mortality *** family E member 2.SERPINE2.has been reported to play a key role in the metastasis of many *** this study,we aimed to investigate the potential mechanism of SERPINE2.in liver cancer ***:The Cancer Genome Atlas database(TCGA),including DNA methy-lation and transcriptome sequencing data,was utilized to identify the crucial oncogene associated with DNA methylation and cancer progression in liver *** from the TCGA and RNA sequencing for 94 pairs of liver cancer tissues were used to explore the correlation between SERPINE2.expression and clin-ical parameters of *** methylation sequencing was used to detect the DNA methylation levels in liver cancer tissues and *** sequencing,cytokine assays,immunoprecipitation(IP)and mass spectrometry(MS)assays,protein stability assays,and ubiquitination assays were performed to explore the regulatory mechanism of SERPINE2.in liver cancer ***-derived xenografts and tumor organoid models were established to determine the role of SERPINE2.in the treatment of liver cancer using ***:Based on the public database screening,SERPINE2.was identified as a tumor promoter regulated by DNA ***2.expression was significantly higher in liver cancer tissues and was associated with the dismal prognosis in patients with liver ***2.promoted liver cancer metas-tasis by enhancing cell pseudopodia formation,cell adhesion,cancer-associated fibroblast activation,extracellular matrix remodeling,and ***/MS assays confirmed that SERPINE2.activated epidermal growth factor receptor(EGFR)and its downstream signaling pathways by interacting with ***,SERPINE2.inhibited EGFR ubiquitination and maintained its protein stability by competing with the E3 ubiquitin ligase,***,EGFR was activated in liver cancer cells after sorafenib treatment,and SER

关键词： liver cancer metastasis DNA methylation SERPINE2 EGFR c-Cbl ubiquitination

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The lysine methyltransferase SMYD2.facilitates neointimal hyperplasia by regulating the HDAC3-SRF axis

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Acta Pharmaceutica Sinica B 2024年第2期14卷 712-728页

作者： Xiaoxuan Zhong Xiang Wei Yan Xu Xuehai Zhu Bo Huo Xian Guo Gaoke Feng Zihao Zhang Xin Feng Zemin Fang Yuxuan Luo Xin Yi Ding-Sheng Jiang Division of Cardiovascular Surgery Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China key laboratory of {2. transplantation Ministry of EducationNHC Key Laboratory of Organ TransplantationChinese Academy of Medical SciencesWuhan 430030China School of Life Science and Technology Key Laboratory of Developmental Genes and Human DiseaseSoutheast UniversityNanjing 210096China Department of Cardiology Renmin Hospital of Wuhan UniversityWuhan 430060China

Coronary restenosis is an important cause of poor long-term prognosis in patients with coronary heart ***,we show that lysine methyltransferase SMYD2.expression in the nucleus is significantly elevated in serum-and PDGF-BB-induced vascular smooth muscle cells(VSMCs),and in tissues of carotid artery injury-induced neointimal ***2.overexpression in VSMCs(Smyd2.vTg)facilitates,but treatment with its specific inhibitor LLY-507 or SMYD2.knockdown significantly inhibits VSMC phenotypic switching and carotid artery injury-induced neointima formation in *** sequencing revealed that SMYD2.knockdown represses the expression of serum response factor(SRF)target genes and that SRF overexpression largely reverses the inhibitory effect of SMYD2.knockdown on VSMC ***3 directly interacts with and deacetylates SRF,which enhances SRF transcriptional activity in ***,SMYD2.promotes HDAC3 expression via tri-methylation of H3K36 at its ***966,a specific inhibitor of HDAC3,not only counteracts the pro-proliferation effect of SMYD2.overexpression on VSMCs,but also inhibits carotid artery injury-induced neointima formation in ***3 partially abolishes the inhibitory effect of SMYD2.knockdown on VSMC proliferation in a deacetylase activity-dependent *** results reveal that the SMYD2.HDAC3-SRF axis constitutes a novel and critical epigenetic mechanism that regulates VSMC phenotypic switching and neointimal hyperplasia.

关键词： Neointimaformation Histonemethylation Histoneacetylation SRFacetylation SMYD2 HDAC3 LLY-507 RGFP966

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A Single-Cell Landscape of Human Liver transplantation Reveals a Pathogenic Immune Niche Associated with Early Allograft Dysfunction

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Engineering 2024年第5期36卷 193-208页

作者： Xin Shao Zheng Wang Kai Wang Xiaoyan Lu Ping Zhang Rongfang Guo Jie Liao Penghui Yang Shusen Zheng Xiao Xu Xiaohui Fan Pharmaceutical Informatics Institute College of Pharmaceutical SciencesZhejiang UniversityHangzhou 310058China National key laboratory of Chinese Medicine Modernization Innovation Center of Yangtze River DeltaZhejiang UniversityJiaxing 314103China Zhejiang University School of Medicine Hangzhou 310058China NHC key laboratory of {2. multi-organ transplantation Hangzhou 310003China Department of Hepatobiliary and Pancreatic Surgery Shulan(Hangzhou)Hospital Affiliated to Shulan International Medical CollegeZhejiang Shuren UniversityHangzhou 310000China Engineering Research Center of Innovative Anticancer Drugs Ministry of EducationHarbin 150023China

Liver transplantation(LT)is the standard therapy for individuals afflicted with end-stage liver *** notable advancements in LT technology,the incidence of early allograft dysfunction(EAD)remains a critical concern,exacerbating the current organ shortage and detrimentally affecting the prognosis of ***,the perplexing hepatic heterogeneity has impeded characterization of the cellular traits and molecular events that contribute to ***,we constructed a pioneering single-cell transcriptomic landscape of human transplanted livers derived from non-EAD and EAD patients,with 12.liver samples collected from 7 donors during the cold perfusion and portal reperfusion *** of the 752.1 cells of non-EAD and EAD patients revealed an EAD-associated immune niche comprising mucosal-associated invariant T cells,granzyme B^(+)(GZMB^(+))granzyme K^(+)(GZMK^(+))natural killer cells,and S100 calcium binding protein A12.(+)(S100A12.(+))***,we verified this immune niche and its association with EAD occurrence in two independent *** findings elucidate the cellular characteristics of transplanted livers and the EAD-associated pathogenic immune niche at the single-cell level,thus,offering valuable insights into EAD onset.

关键词： Human liver transplantation Early allograft dysfunction Pathogenic immune niche Single-cell analysis Cell-cell communication

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Current status and challenges of pig-to-human organ xenotransplantation

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Science China(Life Sciences) 2024年第4期67卷 829-831页

作者： Minghui Fang Yong-Guang Yang Zheng Hu key laboratory of {2. Regeneration&transplantation of Ministry of Education and National-Local Joint Engineering Laboratory of Animal Models for Human DiseasesThe First Hospital of Jilin UniversityChangchun 130061China

organ shortage is a global *** collected by the Global Observatory on Donation and transplantation reveals that over 150,000 solid organ transplants are conducted globally each year,a 52.increase from 2.10(http://***/... 详细信息

关键词： globally global shortage

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Genetic engineering drives the breakthrough of pig models in liver disease research

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Liver Research 2024年第3期8卷 131-140页

作者： Chenhao Xu Xixi Fang Xiao Xu Xuyong Wei Zhejiang University School of Medicine HangzhouZhejiangChina Department of Hepatobiliary and Pancreatic Surgery Hangzhou First People’s HospitalHangzhouZhejiangChina key laboratory of Integrated Oncology and Intelligent Medicine of Zhejiang Province HangzhouZhejiangChina Hangzhou Normal University HangzhouZhejiangChina School of Clinical Medicine Hangzhou Medical CollegeHangzhouZhejiangChina NHC key laboratory of {2. multi-organ transplantation HangzhouZhejiangChina Institute of Translational Medicine Zhejiang UniversityHangzhouZhejiangChina

Compared with the widely used rodents,pigs are anatomically,physiologically,and genetically more similar to humans,making them high-quality models for the study of liver ***,we review the latest research progress on pigs as a model of human liver disease,including methods for establishing them and their advantages in studying cystic fibrosis liver disease,acute liver failure,liver regeneration,non-alcoholic fatty liver disease,liver tumors,and *** also emphasize the importance of genetic engineering techniques,mainly the CRISPR/Cas9 system,which has greatly enhanced the utility of porcine models as a tool for substantially advancing liver disease *** engineering is expected to propel the pig as one of the irreplaceable animal models for future biomedical research.

关键词： Animal model Liver disease Genetic engineering CRISPR/Cas9 Xenogeneic liver transplantation Pig

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