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ZBP1 mediates interferon-induced necroptosis

Cellular & Molecular Immunology 2020年第4期17卷 356-368页

作者： Daowei Yang Yaoji Liang Shubo Zhao Yan Ding Qiuyu Zhuang Qilin Shi Tingting Ai Su-Qin Wu Jiahuai Han State Key Laboratory of Cellular Stress Biology Innovation Center for Cell Signaling NetworkSchool of Life SciencesXiamen UniversityXiamen 361005 FujianChina Department of Cancer Prevention Diagnosis and Treatment Cancer HospitalThe First Affiliated Hospital of Xiamen UniversityTeaching Hospital of Fujian Medical UniversityXiamenChina School of Pharmaceutical Sciences Xiamen UniversityXiamen 361102 FujianChina XMU School of Pharmaceutical Sciences-Amogene Joint R&D Center for Genetic Diagnostics Amogene BiotechXiamen 361102 FujianChina

Interferons(IFNs)play an important role in immunomodulatory and antiviral functions.IFN-induced necroptosis has been reported in cells deficient in receptor-interacting protein kinase 1(RIPK1),Fas-associated protein with death domain(FADD),or caspase-8,but the mechanism is largely unknown.Here,we report that the DNA-dependent activator of IFN regulatory factors(ZBP1,also known as DAI)is required for both type Ⅰ(β)and type Ⅱ(γ)IFN-induced necroptosis.We show that L929 fibroblast cells became susceptible to IFN-induced necroptosis when RIPK1,FADD,or Caspase-8 was genetically deleted,confirming the antinecroptotic role of these proteins in IFN signaling.We found that the pronecroptotic signal from IFN stimulation depends on new protein synthesis and identified ZBP1,an IFN-stimulated gene(ISG)product,as the de novo synthesized protein that triggers necroptosis in IFN-stimulated cells.The N-terminal domain(ND)of ZBP1 is important for ZBP1–ZBP1 homointeraction,and its RHIM domain in the C-terminal region interacts with RIPK3 to initiate RIPK3-dependent necroptosis.The antinecroptotic function of RIPK1,FADD,and caspase-8 in IFN-treated cells is most likely executed by caspase-8-mediated cleavage of RIPK3,since the inhibitory effect on necroptosis was eliminated when the caspase-8 cleavage site in RIPK3 was mutated.ZBP1-mediated necroptosis in IFN-treated cells is likely physiologically relevant,as ZBP1 KO mice were significantly protected against acute systemic inflammatory response syndrome(SIRS)induced by TNF+IFN-γ.

关键词： ZBP1 interferon necroptosis

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Targeting necroptosis in anticancer therapy:mechanisms and modulators

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Acta Pharmaceutica Sinica B 2020年第9期10卷 1601-1618页

作者： Ying Wu Guoqiang Dong Chunquan Sheng School of Pharmacy Second Military Medical UniversityShanghai 200433China School of Pharmaceutical Sciences Zhengzhou UniversityZhengzhou 450001China

necroptosis,a genetically programmed form of necrotic cell death,serves as an important pathway in human diseases.As a critical cell-killing mechanism,necroptosis is associated with cancer progression,metastasis,and immunosurveillance.Targeting necroptosis pathway by small molecule modulators is emerging as an effective approach in cancer therapy,which has the advantage to bypass the apoptosis-resistance and maintain antitumor immunity.Therefore,a better understanding of the mechanism of necroptosis and necroptosis modulators is necessary to develop novel strategies for cancer therapy.This review will summarize recent progress of the mechanisms and detecting methods of necroptosis.In particular,the relationship between necroptosis and cancer therapy and medicinal chemistry of necroptosis modulators will be focused on.

关键词： Cell death necroptosis Inducers Inhibitors Anticancer therapy

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Dabrafenib,an inhibitor of RIP3 kinase-dependent necroptosis,reduces ischemic brain injury

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Neural Regeneration Research 2018年第2期13卷 252-256页

作者： Shelly A.Cruz Zhaohong Qin Alexandre E R.Stewart Hsiao-Huei Chen Ottawa Hospital Research Institute OttawaCanada University of Ottawa Brain and Mind InstituteOttawaCanada University of Ottawa Heart Institute OttawaCanada Canadian Partnership for Storke Recovery OttawaCanada

Ischemic brain injury triggers neuronal cell death by apoptosis via caspase activation and by necroptosis through activation of the receptor-interacting protein kinases （RIPK） associated with the tumor necrosis factor-alpha （TNF-a）/death receptor. Recent evidence shows RIPK inhibitors are neuroprotective and al- leviate ischemic brain injury in a number of animal models, however, most have not yet undergone clinical trials and safety in humans remains in question. Dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar con- centrations. Here, we investigated whether Dabrafenib would show a similar neuroprotective effect in mice subjected to ischemic brain injury by photothrombosis. Dabrafenib administered intraperitoneally at 10 mg/ kg one hour after photothrombosis-induced focal ischemic injury significantly reduced infarct lesion size in C57BL6 mice the following day, accompanied by a markedly attenuated upregulation of TNF-u. However, subsequent lower doses （5 mg/kg/day） failed to sustain this neuroprotective effect after 4 days. Dabrafenib bl ocked lipopolysaccharides-induced activation of TNF-ct in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-ct-induced necroptotic pathway after ischemic brain injury. Since Dab- rafenib is already in clinical use for the treatment of melanoma, it might be repurposed for stroke therapy.

关键词： ischemic brain injury inflammation macrophage Dabrafenib tumor necrosis factor-alpha photothrombosis receptor-interacting protein kinases necroptosis microgIia stroke neural regeneration

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Implications of necroptosis for Cardiovascular Diseases

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Current Medical Science 2019年第4期39卷 513-522页

作者： Zhao-hui RUAN Zi-xuan XU Xue-yun ZHOU Xian ZHANG Lei SHANG Jiangxi Research Institute of Ophthalmology and Visual Sciences Affiliated Eye Hospital of Nanchang UniversityNanchang

necroptosis is a non-apoptotic programmed cell death pathway,which causes necrosislike morphologic changes and triggers inflammation in the surrounding tissues.Accumulating evidence has demonstrated that necroptosis is involved in a number of pathological processes that lead to cardiovascular diseases.However,the exact molecular pathways linking them remain unknown.Herein,this review summarizes the necroptosis-related pathways involved in the development of various cardiovascular diseases,including atherosclerosis,cardiac ischemia-reperfusion injury,cardiac hypertrophy,dilated cardiomyopathy and myocardial infarction,and may shed light on the diagnosis and treatment of these diseases.

关键词： cell death death-associated molecular patterns necroptosis cardiovascular disease

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Cross electro-nape-acupuncture ameliorates cerebral hemorrhageinduced brain damage by inhibiting necroptosis

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World Journal of Clinical Cases 2020年第10期8卷 1848-1858页

作者： Guo-Feng Cai Zhong-Ren Sun Zhe Zhuang Hai-Chun Zhou Shan Gao Kai Liu Li-Li Shang Kun-Ping Jia Xiu-Zhen Wang Hui Zhao Guo-Liang Cai Wen-Li Song Sheng-Nan Xu Hanan Branch of Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine Harbin 150001Heilongjiang ProvinceChina Postdoctoral Research Station of Heilongjiang Academy of Traditional Chinese Medicine Harbin 150001Heilongjiang ProvinceChina Heilongjiang University of Traditional Chinese Medicine Harbin 150040Heilongjiang ProvinceChina Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine Harbin 150000Heilongjiang ProvinceChina First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine Harbin 150040Heilongjiang ProvinceChina Harbin Sport University Harbin 150001Heilongjiang ProvinceChina Graduate School of Heilongjiang University of Traditional Chinese Medicine Harbin 150040Heilongjiang ProvinceChina

BACKGROUND Receptor interacting protein kinase 1(RIPK1)-mediated cell death,including apoptosis and necroptosis,belongs to programmed cell death.It has been reported that RIPK1-mediated necroptosis exists in lesions of cerebral hemorrhage(CH).Electroacupuncture,a treatment derived from traditional Chinese medicine,could improve neurological impairment in patients with brain injury.AIM To investigate the protective role of cross electro-nape acupuncture(CENA)in CH,and clarify the potential mechanism.METHODS CH rat models were established,and CENA was applied to the experimental rats.Neurological functions and encephaledema were then measured.Necrotic cells in the brain of rats with CH were evaluated by propidium iodide staining.necroptosis was assessed by immunofluorescence.Activation of the necroptosisrelated pathway was detected by western blot.Extraction of brain tissue,cerebrospinal fluid and serum samples was conducted to measure the expression and secretion of inflammatory cytokines by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay.RESULTS The necroptotic marker p-MLKL was detectable in the brains of rats with CH.Next,we found that CENA could ameliorate neurological functions in rat models of CH.Moreover,the upregulation of RIPK1-mediated necroptosis-related molecules in the brains of rats with CH were inhibited by CENA.Further investigation revealed that CENA partially blocked the interaction between RIPK1 and RIPK3.Finally,in vivo assays showed that CENA decreased the expression of the inflammatory cytokines tumor necrosis factor-α,interleukin-6 and interleukin-8 in CH rat models.CONCLUSION These findings revealed that CENA exerts a protective role in CH models by inhibiting RIPK1-mediated necroptosis.

关键词： Cross electro-nape acupuncture Cerebral hemorrhage Receptor interacting protein kinase 1 necroptosis Quantitative real-time polymerase chain reaction Enzymelinked immunosorbent assay

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Compartmentalized necroptosis activation in excitotoxicityinduced axonal degeneration: a novel mechanism implicated in neurodegenerative disease pathology

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Neural Regeneration Research 2019年第8期14卷 1385-1386页

作者： Macarena S. Arrazola Felipe A. Court Center for Integrative Biology Faculty of Sciences Universidad Mayor de Chile Santiago CnileFONDAP Center for Geroscience Brain Health and Metabolism Santiago Chile Buck Institute for Research on Ageing Novato San Francisco CA USA

Excitotoxicity and neuronal cell death: Glutamate is the main excitatory neurotransmitter of the central nervous system and functionally involved in most brain activities, including brain development, synaptic plasticity, learning and memory. Exc让atory synaptic transmission is primarily mediated by ligana-gated ion channels, including a-amino-3-hydroxy-5-methylisoxazoIe-4-propionic acid (AMPA), N-methyl-D-aspartate (NMDA) and kainate receptors. Activation of glutamate receptors, particularly NMDA receptors, usually leads to calcium influx, whicn can act as a second messenger for several processes to mediate synaptic activity and brain function. Nevertheless, excessive release of glutamate neurotransmitter may produce intracellular calcium overload, leading to a cascade of events mediating cytoskeleton damage accompanied w让h reactive oxygen species (ROS) generation, mitochondrial dysfunction and ultimately neuronal cell death. These toxic effects of glutamate are known as excitotoxicity. Neuronal excitotoxicity has been linked to several acute and chronic brain diseases, such as stroke/ischemia, epilepsy and a range of neurodegenerative disorders, including Alzheimer's disease (AD), Huntingtons disease, amyotrophic lateral sclerosis (ALS) and Parkinsons disease (PD), contributing to the neuronal lost in different brain regions. Unfortunately, treating nervous system disorders with general glutamate receptor blockers has been associated with undesirable side effects, becoming increasingly necessary to unravel downstream effectors in the excitotoxicity-dependent cell death pathway in order to develop novel therapeutic strategies.

关键词： Compartmentalized necroptosis activation excitotoxicityinduced axonal neurodegenerative disease

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Activation of autophagy in photoreceptor necroptosis after experimental retinal detachment

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International Journal of Ophthalmology(English edition) 2014年第5期7卷 745-752页

作者： Kai Dong Zi-Cheng Zhu Feng-Hua Wang Gen-Jie Ke Zhang Yu Xun Xu Department of Ophthalmology Anhui Provincial HospitalAnhui Medical University Department of Ophthalmology Shanghai First People's HospitalSchool of MedicineShanghai Jiaotong University Eye Research Institute of Shanghai Jiaotong University Department of Morphology Fudan University Shanghai Medical College Department of Ophthalmology Shanghai First People's HospitalSchool of Medicine Shanghai Jiaotong University Shanghai Key Laboratory of Fundus Disease

AIM:To investigate whether photoreceptor necroptosis induced by z-VAD-FMK(pan caspase inhibitor) was involved the activation of autophagy and whether Necrostatin-1, a specific necroptosis inhibitor, could inhibit this induction of autophagy after experimental retinal detachment.METHODS:Experimental retinal detachment models were created in Sprague-Dawley rats by subretinal injection of sodium hyaluronate and subretinal injections of z-VAD-FMK, vehicle or z-VAD-FMK plus Necrostatin-1.Three days after retinal detachment, morphologic changes were observed by transmission electron microscopy. In other animals, retinas were subjected to immunoprecipitation and Western Blotting, then probed with anti-RIP1, phosphoserine, LC-3II or caspase 8antibody.RESULTS:It was proved by immunoprecipitation and western blotting, that photoreceptor necroptosis was mediated by caspase-8 inhibition and receptor interacting protein kinase(RIP1) phosphorylation activation. Transmission electron microscope and western blotting results indicated that photoreceptornecroptosis was involved the LC-3II and autophagosomes induction. We also discovered Necrostatin-1 could inhibit RIP1 phosphorylation and LC-3II induction.CONCLUSION:These data firstly indicate photoreceptor necroptosis is associated with the activation of autophagy. Necrostatin-1 protects photoreceptors from necroptosis and autophagy by down-regulation of RIP1 phosphorylation and LC-3II.

关键词： retinal detachment autophagy necroptosis

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necroptosis in ischemia-reperfusion injury of lean and steatotic livers

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Liver Research 2019年第3期3卷 227-233页

作者： Hua Sun Tara McKeen Hua Wang Hong-Min Ni Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKSUSA Department of Oncology The First Affiliated Hospital of Anhui Medical UniversityHefeiAnhuiChina

Hepatic ischemia-reperfusion(IR)injury is a major complication during liver transplantation,liver resection,and other clinical situations.Increased hepatic IR injury in steatotic livers is a major reason for rejecting the use of steatotic livers for liver transplantation.necroptosis is implicated in the pathogenesis of fatty liver diseases,including non-alcoholic fatty liver disease(NAFLD)and alcoholic liver disease(ALD).necroptosis is one type of regulated cell death and is regulated by three key proteins:receptorinteracting protein 1(RIP1),receptor-interacting protein 3(RIP3),and mixed-lineage kinase domainlike protein(MLKL).In this review,we examine the necroptosis status in the steatotic liver diseases NAFLD and ALD as well as its role in hepatic IR injury of lean and steatotic livers.

关键词： necroptosis Non-alcoholic fatty liver disease(NAFLD) Alcoholic liver disease(ALD) Ischemia-reperfusion(IR) Liver injury

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Construction of prognostic model of cervical cancer based on necroptosis-related lncRNAs

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Medical Data Mining 2022年第3期5卷 23-35页

作者： Jin Cao Bu-Hai Wang Yi-Chen Liang J.Juan Gu Yu-Xiang Huang Medical College Yangzhou UniversityYangzhou 225000China Institute of Oncology Northern Jiangsu People's HospitalYangzhou 225000China Department of Oncology Northern Jiangsu People's HospitalYangzhou 225000China

Background:Long non-coding RNAs(lncRNAs)can influence the necroptosis process,which is essential in malignant tumors.But no studies have looked at the predictive value of necroptosis-related lncRNAs in cervical cancer(CC).Using necroptosis-related lncRNAs,we developed a prediction signature to predict the prognosis of CC patients.Method:We gathered the RNA-seq and related clinical data for patients with CC from the Cancer Genome Atlas(TCGA)database.To identify lncRNAs linked to necroptosis,we then conducted univariate and multivariate Cox regression analyses.Co-expression network analysis,least absolute shrinkage selection operator(LASSO)regression analysis and multivariate Cox regression analyses were subsequently used to further filter necroptosis-related lncRNAs signature and construct a predictive model.Finally,we examined the medication sensitivity between the two risk groups.We performed a single-sample gene set enrichment analysis(ssGSEA)to investigate the association between the predictive signature and the tumor immune microenvironment.Result:Six necroptosis-related lncRNAs(AL021807.1,AC026803.2,AC015819.1,AC233728.1,AL158166.1,NKILA)that are independently connected to the overall survival(OS)time of CC patients make up the signature we created.For predicting the 1-,3-,and 5-year survival rates,the areas under the receiver operating characteristic(ROC)curve(AUC)were 0.72,0.791,and 0.808.It was determined that the risk score model was a separate prognostic component.The Kaplan-Meier analysis revealed that the prognosis for CC patients in the high-risk category was worse.Low-risk CC patients had more active immune systems and responded better to PD1/L1 immunotherapy.Conclusion:The signature based on necroptosis-related lncRNAs is a reliable biomarker,which is more likely to independently predict the prognosis of patients with CC and offer a foundation for the pathogenesis of necroptosis-related lncRNAs in CC.It can also be utilized to direct the tailored therapy of CC patients.

关键词： cervical cancer necroptosis long noncoding RNAs prognostic signature the cancer genome atlas

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Based on necroptosis identifying the immunological features and prognostic signatures of lung adenocarcinoma

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Medical Data Mining 2022年第2期5卷 16-27页

作者： Peng Xia De-Gui Wang Si-Wei Ouyang Rong Shen Zhao Guo Xu-Guang Yang Xiang-Wen Liu Kun Xie Department of Anatomy and Histology School of Basic Medical SciencesLanzhou UniversityLanzhou 730030China

Background:Lung adenocarcinoma is one of the most common pathological types of lung malignant tumor with high morbidity and mortality.Long non-coding RNAs are gradually recognized to play crucial roles in tumor occurrence and development.necroptosis is a newly established way for cell programmed death,undertaking essential roles in anti-tumor.Therefore,identifying necroptosis-related l ong non-coding RNAs and based on them to evaluate the signatures of l ung adenocarcinoma is essential for patients’survival prediction and therapy.Methods:We collected data from the public database and performed the least absolute shrinkage to construct a 13-lncRNAs prognostic model.Based on the Consensus Clustering,ESTIMATE,CIRERSORT,and weighted gene co-expression network analysis to identify the immune signatures.Results:This study identified a 13-lncRNAs prognostic model.The model’s prediction accuracy was evaluated by receiver operating characteristic and independent-prognosis analysis;besides,a Gene Expression Omnibus dataset was applied for external validation.Furthermore,we analyzed the immune features of subgroups in multiple dimensions.A consensus clustering analysis based on the 41 genes was implemented to separate lung adenocarcinoma patients into two subgroups.We compared the features of subgroups in multiple dimensions,including survival,immune microenvironment,immune cells infiltration and gene co-expression network analysis.Conclusion:W e established a prognosis necroptosis-related risk model to predict lung adenocarcinoma patients’prognosis and systematically understood the correlation between immune and necroptosis.This study can applicate in clinical to predict the prognosis of lung adenocarcinoma patients and provide new insight into lung adenocarcinoma immune therapy.

关键词： lung adenocarcinoma l ong non-coding RNAs necroptosis the least absolute shrinkage and selection operator prognostic model

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