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Disulfiram, an aldehyde dehydrogenase inhibitor, works as a potent drug against sepsis and cancer via NETosis, pyroptosis, apoptosis, ferroptosis, and cuproptosis

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Blood Science 2022年第3期4卷 152-154页

作者： Dingrui Nie Cunte Chen Yangqiu Li Chengwu Zeng key laboratory for regenerative medicine of ministry of education Institute of HematologySchool of MedicineJinan UniversityGuangzhouChina

Regulated cell death(RCD)is essential for maintaining cell homeostasis and preventing diseases.Besides classical apoptosis,several novel nonapoptotic forms of RCD including NETosis,pyroptosis,ferroptosis,and cuproptosis have been reported and are increasingly being implicated in various cancers and inflammation.Disulfiram(DSF),an aldehyde dehydrogenase inhibitor,has been used clinically for decades as an anti-alcoholic drug.New studies have shown that DSF possesses potent anti-inflammatory and anti-cancer effects by regulating these new types of RCD.Here,we summarize the mechanisms and discuss the potential application of DSF in the treatment of cancers and inflammatory diseases.

关键词： Apoptosis Cuproptosis Disulfiram Ferroptosis Sepsis NETosis Pyroptosis

Membrane dynamics of ATG4B and LC3 in autophagosome formation

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Journal of Molecular Cell Biology 2021年第12期13卷 853-863页

作者： Yuanyuan Zhou Zhenkun Wang Yijia Huang Chujie Bai Xianli Zhang Mengdie Fang Zhenyu Ju Bo Liu Key Laboratory of Regenerative Medicine of Ministry of Education Guangzhou Regenerative Medicine and Health Guangdong LaboratoryInstitute of Aging and Regenerative MedicineJinan UniversityGuangzhou 510632China key laboratory of Carcinogenesis and Translational Research(ministry of education/Beijing) Department of Bone and Soft Tissue TumorPeking University Cancer Hospital and InstituteBeijing 100142China College of Bioengineering Hangzhou Medical CollegeHangzhou 310013China

The biogenesis of autophagosomes provides the basis for macroautophagy to capture and degrade intracellular cargoes.Binding of the autophagy-related protein ATG8/LC3 to autophagic membranes is essential to autophagosome formation,which involves the specific and dynamic processing of ATG8/LC3 by cysteine protease ATG4.However,to date,the mechanism whereby ATG4 is recruited to the membranes,the interaction of ATG4 and ATG8/LC3 on the membranes,and its role in the growth of phagophore are not completely understood.Here,we used fluorescence recovery after photobleaching to monitor the turnover of GFP-tagged ATG4B and LC3B in living animal cells.The data show that ATG4B localizes to early autophagic membranes in an LC3B-dependent manner.During autophagy,ATG4B and LC3B undergo rapid cytosol/isolation membrane exchange but not at the cytosol/completed autophagosome.In addition,ATG4B activity controls the efficiency of autophagosome formation by impacting the membrane binding/dissociation of LC3B.These data suggest that ATG4 and LC3 play interdependent roles in the formation of autophagosomes.

关键词： autophagy autophagosome biogenesis ATG4 LC3 live-cell imaging membrane binding kinetics

The gene expression patterns of BMPR2,EP300,TGFβ2,and TNFAIP3 in B-Lymphoma cells

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Cancer Biology & medicine 2014年第3期11卷 202-207页

作者： Dong-Mei He Hong Wu Xiu-Li Wu Li Ding Ling Xu Yang-Qiu Li Institute of Hematology Medical College key laboratory for regenerative medicine of ministry of education Jinan University

Objective: The results of a previous study showed that a clear dysregulation was evident in the global gene expression of the BCL11A-suppressed B-lymphoma cells. In this study, the bone morphogenetic protein receptor, type II(BMPR2), E1 A binding protein p300(EP300), transforming growth factor-β2(TGFβ2), and tumor necrosis factor, and alpha-induced protein 3(TNFAIP3) gene expression patterns in B-cell malignancies were studied. Methods: The relative expression levels of BMPR2, EP300, TGFβ2, and TNFAIP3 mRNA in B-lymphoma cell lines, myeloid cell lines, as well as in cells from healthy volunteers, were determined by real-time quantitative reverse transcriptpolymerase chain reaction(qRT-PCR) with SYBR Green Dye. Glyceraldehyde-3-phosphate dehydrogenase(GAPDH) was used as reference. Results: The expression level of TGFβ2 mRNA in B-lymphoma cell lines was significantly higher than those in the cells from the healthy control(P0.05). In B-lymphoma cell lines, correlation analyses revealed that the expression of BMPR2 and TNFAIP3(r=0.882, P=0.04) had significant positive relation. The expression levels of BMPR2, EP300, and TNFAIP3 mRNA in cell lines from myeloid leukemia were significantly lower than those in the cells from the healthy control(P0.05). The expression levels of BMPR2, EP300, and TNFAIP3 mRNA in B-lymphoma cells were significantly higher than those of the myeloid leukemia cells(P<0.05).Conclusion: Different expression patterns of BMPR2, EP300, TGFβ2, and TNFAIP3 genes in B-lymphoma cells exist.

关键词：白血病细胞系 B细胞淋巴瘤基因表达模式 TGFβ2 mRNA表达水平甘油醛-3-磷酸脱氢酶骨形态发生蛋白恶性肿瘤

Ferrostatin-1 protects HT-22 cells from oxidative toxicity

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Neural Regeneration Research 2020年第3期15卷 528-536页

作者： Jun Chu Chen-Xu Liu Rui Song Qing-Lin Li Xin’an key laboratory of medicine Ministry of Education Anhui University of Chinese Medicine

Ferroptosis is a type of programmed cell death dependent on iron.It is different from other forms of cell death such as apoptosis,classic necrosis and autophagy.Ferroptosis is involved in many neurodegenerative diseases.The role of ferroptosis in glutamate-induced neuronal toxicity is not fully understood.To test its toxicity,glutamate(1.25–20 mM)was applied to HT-22 cells for 12 to 48 hours.The optimal experimental conditions occurred at 12 hours after incubation with 5 mM glutamate.Cells were cultured with 3–12μM ferrostatin-1,an inhibitor of ferroptosis,for 12 hours before exposure to glutamate.The cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Autophagy was determined by monodansylcadaverine staining and apoptosis by caspase 3 activity.Damage to cell structures was observed under light and by transmission electron microscopy.The release of lactate dehydrogenase was detected by the commercial kit.Reactive oxygen species were measured by flow cytometry.Glutathione peroxidase activity,superoxide dismutase activity and malondialdehyde level were detected by the appropriate commercial kit.Prostaglandin peroxidase synthase 2 and glutathione peroxidase 4 gene expression was detected by real-time quantitative polymerase chain reaction.Glutathione peroxidase 4 and nuclear factor erythroid-derived-like 2 protein expression was detected by western blot analysis.Results showed that ferrostatin-1 can significantly counter the effects of glutamate on HT-22 cells,improving the survival rate,reducing the release of lactate dehydrogenase and reducing the damage to mitochondrial ultrastructure.However,it did not affect the caspase-3 expression and monodansylcadaverine-positive staining in glutamate-injured HT-22 cells.Ferrostatin-1 reduced the levels of reactive oxygen species and malondialdehyde and enhanced superoxide dismutase activity.It decreased gene expression of prostaglandin peroxidase synthase 2 and increased gene expression of glutathione peroxidase 4 and protein ex

关键词： ferroptosis ferrostatin-1 glutamate glutathione peroxidase 4 HT-22 cell oxidative toxicity prostaglandin peroxidase synthase 2 reactive oxygen species

Autophagy regulation combined with stem cell therapy for treatment of spinal cord injury

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Neural Regeneration Research 2023年第8期18卷 1629-1636页

作者： Yao Shen Yi-Piao Wang Xin Cheng Xuesong Yang Guang Wang Division of Histology and Embryology International Joint Laboratory for Embryonic Development&Prenatal MedicineMedical CollegeJinan UniversityGuangzhouGuangdong ProvinceChina key laboratory for regenerative medicine of the ministry of education Jinan UniversityGuangzhouGuangdong ProvinceChina

Stem cells are a group of cells with unique self-renewal and differentiation abilities that have great prospects in the repair of spinal cord injury. However, stem cell renewal and differentiation require strict control of protein turnover in the stem cells to achieve cell remodeling. As a highly conserved “gatekeeper” of cell homeostasis, autophagy can regulate cell remodeling by precisely controlling protein turnover in cells. Recently, it has been found that the expression of autophagy markers changes in animal models of spinal cord injury. Therefore, understanding whether autophagy can affect the fate of stem cells and promote the repair of spinal cord injury is of considerable clinical value. This review expounds the importance of autophagy homeostasis control for the repair of spinal cord injury from three aspects—pathophysiology of spinal cord injury, autophagy and stem cell function, and autophagy and stem cell function in spinal cord injury—and proposes the synergistic therapeutic effect of autophagy and stem cells in spinal cord injury.

关键词： autophagy chaperone-mediated autophagy embryonic stem cells induced pluripotent stem cells inflammation mesenchymal stem cells neural stem cells oxidative stress spinal cord injury

The E3 ubiquitin ligase NEDD4-1 protects against acetaminophen-induced liver injury by targeting VDAC1 for degradation

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Acta Pharmaceutica Sinica B 2023年第4期13卷 1616-1630页

作者： Yiwei Zhu Lin Lei Xinghui Wang Linfang Chen Wei Li Jinxia Li Chenchen Zhao Xiliang Du Yuxiang Song Wenwen Gao Guowen Liu Xinwei Li State key laboratory for Zoonotic Diseases Key Laboratory of Zoonosis ResearchMinistry of EducationCollege of Veterinary MedicineJilin UniversityChangchun 130062China

Acetaminophen(APAP)overdose is a major cause of liver injury.Neural precursor cell expressed developmentally downregulated 4—1(NEDD4-1)is an E3 ubiquitin ligase that has been implicated in the pathogenesis of numerous liver diseases;however,its role in APAP-induced liver injury(AILI)is unclear.Thus,this study aimed to investigate the role of NEDD4-1 in the pathogenesis of AILI.We found that NEDD4-1 was dramatically downregulated in response to APAP treatment in mouse livers and isolated mouse hepatocytes.Hepatocyte-specific NEDD4-1 knockout exacerbated APAP-induced mitochondrial damage and the resultant hepatocyte necrosis and liver injury,while hepatocyte-specific NEDD4-1 overexpression mitigated these pathological events both in vivo and in vitro.Additionally,hepatocyte NEDD4-1 deficiency led to marked accumulation of voltage-dependent anion channel 1(VDAC1)and increased VDAC1 oligomerization.Furthermore,VDAC1 knockdown alleviated AILI and weakened the exacerbation of AILI caused by hepatocyte NEDD4-1 deficiency.Mechanistically,NEDD4-1 was found to interact with the PPTY motif of VDAC1 through its WW domain and regulate K48-linked ubiquitination and degradation of VDAC1.Our present study indicates that NEDD4-1 is a suppressor of AILI and functions by regulating the degradation of VDAC1.

关键词： Acetaminophen NEDD4-1 VDAC1 Liver injury Hepatotoxicity Necrosis Mitochondrial damage Ubiquitination

The dynamic metabolic profile of Qi-Yu-San-Long decoction in rat urine using UPLC-QTOF-MS^(E) coupled with a post-targeted screening strategy

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Journal of Pharmaceutical Analysis 2022年第5期12卷 755-765页

作者： Ting Zheng Yue Zhao Ruijuan Li Mengwen Huang An Zhou Zegeng Li Huan Wu key laboratory of Xin'an medicine Ministry of EducationAnhui University of Chinese MedicineHefei230038China

Qi-Yu-San-Long decoction(QYSLD)is a traditional Chinese medicine that has been clinically used in the treatment of non-small-cell lung cancer(NSCLC)for more than 20 years.However,to date,metabolicrelated studies on QYSLD have not been performed.In this study,a post-targeted screening strategy based on ultra-performance liquid chromatography coupled with quadrupole time-of-flight full information tandem mass spectrometry(UPLC-QTOF-MS^(E))was developed to identify QYSLD-related xenobiotics in rat urine.The chemical compound database of QYSLD constituents was established from previous research,and metabolites related to these compounds were predicted in combination with their possible metabolic pathways.The metabolites were identified by extracted ion chromatograms using predicted m/z values as well as retention time,excimer ions,and fragmentation behavior.Overall,85 QYSLD-related xenobiotics(20 prototype compounds and 65 metabolites)were characterized from rat urine.The main metabolic reactions and elimination features of QYSLD included oxidation,reduction,decarboxylation,hydrolysis,demethylation,glucuronidation,sulfation,methylation,deglycosylation,acetylation,and associated combination reactions.Of the identified molecules,14 prototype compounds and 58 metabolites were slowly eliminated,thus accumulating in vivo over an extended period,while five prototypes and two metabolites were present in vivo for a short duration.Furthermore,one prototype and five metabolites underwent the process of“appearing-disappearing-reappearing”in vivo.Overall,the metabolic profile and characteristics of QYSLD in rat urine were determined,which is useful in elucidating the active components of the decoction in vivo,thus providing the basis for studying its mechanism of action.

关键词： Qi-Yu-San-Long decoction Post-targeted screening strategy Dynamic metabolic profile UPLC-QTOF-MS^(E)

Extensive exploration of T cell heterogeneity in cancers by single cell sequencing

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Chinese Journal of Cancer Research 2019年第2期31卷 410-418页

作者： Xiaofang Wang Yangqiu Li Department of Hematology First Affiliated Hospital School of Medicine Jinan University key laboratory for regenerative medicine of ministry of education Institute of Hematology School of Medicine Jinan University

Human T cells are a highly heterogeneous population and can recognize a wide variety of antigens by their T cell receptors(TCRs). Tumor cells display a large repertoire of antigens that serve as potential targets for recognition,thus making T cells in the tumor micro-environment more complicated. Making a connection between TCRs and the transcriptional information of individual T cells will be interesting for investigating clonal expansion within T cell populations under pathologic conditions. Advances in single cell RNA-sequencing(scRNA-seq) have allowed for comprehensive analysis of T cells. In this review, we briefly describe the research progress on tumor microenvironment T cells using single cell RNA sequencing, and then discuss how scRNA-seq can be used to resolve immune system heterogeneity in health and disease. Finally, we point out future directions in this field and potential for immunotherapy.

关键词： T cells tumor micro-environment single-cell RNA-sequencing

Developmental expression of three prmt genes in Xenopus

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Zoological Research 2019年第2期40卷 102-107页

作者： Cheng-Dong Wang Xiao-Fang Guo Thomas Chi Bun Wong Hui Wang Xu-Feng Qi Dong-Qing Cai Yi Deng Hui Zhao key laboratory for regenerative medicine Ministry of EducationSchool of Biomedical Sciences Faculty of Medicine The Chinese University of Hong Kong key laboratory for regenerative medicine of ministry of medicine of ministry of education Jinan University Department of Developmental & regenerative Biology College of Life Science and Technology Jinan University Guangdong Provincial key laboratory of Cell Microenvironment Department of Biology South University of Science and Technology of China Kunming Institute of Zoology Chinese Academy of Sciences-The Chinese University of Hong Kong Joint Laboratory of Bioresources and Molecular Research of Common Diseases

DEAR EDITOR Protein arginine methyltransferases (PRMTs)are involved in many cellular processes via the arginine methylation of histone or non-histone proteins.We examined the expression patterns of prmt4,prmt7,and prmt9 during embryogenesis in Xenopus using whole-mount in situ hybridization and quantitative reverse transcription polymerase chain reaction (RT-PCR).Xenopus prmt4 and prmt7 were expressed in the neural crest,brain,and spinal cord,and also detected in the eye,branchial arches,and heart at the tailbud stage.Specific print9 signals were not detected in Xenopus embryos until the late tailbud stage when weak expression was observed in the branchial arches.Quantitative RT-PCR indicated that the expression of prmt4 and prmt7 was up-regulated during the neurula stage,whereas prmt9 maintained its low expression until the late tailbud stage,consistent with the whole-mount in situ hybridization results.Thus,the developmental expression patterns of these three print genes in Xenopus embryos provide a basis for further functional study of such genes.

关键词： Developmental expression prmt genes Xenopus