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Insight into crosstalk Between Mitophagy and Apoptosis/Necroptosis:Mechanisms and Clinical Applications in Ischemic Stroke

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Current Medical Science 2022年第2期42卷 237-248页

作者： Yan-di YANG Zi-xin LI Xi-min HU Hao WAN Qi ZHANG Rui XIAO Kun XIONG Department of Anatomy and Neurobiology School of Basic Medical ScienceCentral South UniversityChangsha 410013China Clinical Medicine Eight-year Program 03 Class18 GradeXiangya School of MedicineCentral South UniversityChangsha 410013China Clinical Medicine Eight-Year Program 02 Class17 GradeXiangya School of MedicineCentral South UniversityChangsha 410013China Administrative Office the Third Xiangya HospitalCentral South UniversityChangsha 410013China Hunan Key Laboratory of Ophthalmology Changsha 410008China Key Laboratory of Emergency and Trauma Ministry of EducationCollege of Emergency and TraumaHainan Medical UniversityHaikou 571199China

Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality.As a result of ischemia-reperfusion,a cascade of pathophysiological responses is triggered by the imbalance in metabolic supply and demand,resulting in cell loss.These cellular injuries follow various molecular mechanisms solely or in combination with this disorder.Mitochondria play a driving role in the pathophysiological processes of ischemic stroke.Once ischemic stroke occurs,damaged cells would respond to such stress through mitophagy.Mitophagy is known as a conservatively selective autophagy,contributing to the removal of excessive protein aggregates and damaged intracellular components,as well as aging mitochondria.Moderate mitophagy may exert neuroprotection against stroke.Several pathways associated with the mitochondrial network collectively contribute to recovering the homeostasis of the neurovascular unit.However,excessive mitophagy would also promote ischemia-reperfusion injury.Therefore,mitophagy is a double-edged sword,which suggests that maximizing the benefits of mitophagy is one of the direction of future efforts.This review emphasized the role of mitophagy in ischemic stroke,and highlighted the crosstalk between mitophagy and apoptosis/necroptosis.

关键词： mitophagy ischemic stroke apoptosis necroptosis clinical application crosstalk

crosstalk Aware Register Reallocation Method for Green Compilation

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Computers, Materials & Continua 2020年第6期63卷 1357-1371页

作者： Sheng Xiao Jing Selena He Xi Yang Yazhe Wang Lu Jin Information Science and Engineering Department Hunan First Normal UniversityChangsha410205China Computer School Wuhan UniversityWuhan430072China Department of Computer Science Kennesaw State UniversityKennesaw30144-5588USA Hunan Guangyi Experimental Middle School Changsha410205China

As nanoscale processing becomes the mainstream in IC manufacturing,the crosstalk problem rises as a serious challenge,not only for energy-efficiency and performance but also for security requirements.In this paper,we propose a register reallocation algorithm called Nearby Access based Register Reallocation(NARR)to reduce the crosstalk between instruction buses.The method includes construction of the software Nearby Access Aware Interference Graph(NAIG),using data flow analysis at assembly level,and reallocation of the registers to the software.Experimental results show that the crosstalk could be dramatically minimized,especially for 4C crosstalk,with a reduction of 80.84%in average,and up to 99.99%at most.

关键词： crosstalk energy efficiency register reallocation green compilation

crosstalk analysis of silicon-on-insulator nanowire-arrayed waveguide grating

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Chinese Physics B 2016年第12期25卷 294-299页

作者：李凯丽安俊明张家顺王玥王亮亮李建光吴远大尹小杰胡雄伟 State Key Laboratory on Integrated Optoelectronics Institute of SemiconductorsChinese Academy of Sciences

The factors influencing the crosstalk of silicon-on-insulator （SO1） nanowire arrayed waveguide grating （AWG） are analyzed using the transfer function method. The analysis shows that wider and thicker arrayed waveguides, outsider fracture of arrayed waveguide, and larger channel space, could mitigate the deterioration of crosstalk. The SOI nanowire AWGs with different arrayed waveguide widths are fabricated by using deep ultraviolet lithography （DUV） and inductively coupled plasma etching （ICP） technology. The measurement results show that the crosstalk performance is improved by about 7 dB through adopting 800 nm arrayed waveguide width.

关键词： SOI nanowire AWG crosstalk phase errors

crosstalk-aware RCSA for spatial division multiplexing enabled elastic optical networks with multi-core fibers

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Chinese Optics Letters 2016年第10期14卷 29-33页

作者：朱睿杰赵永利杨辉陈浩然张杰 Jason P. Jue State Key Laboratory of Information Photonics and Optical Communication Beijing University of Posts and Telecommunications Beijing 100876 China University of Texas at Dallas Texas 75080 USA

In this Letter, we propose two crosstalk-aware routing, core, and spectrum assignment （CA-RCSA） algorithms for spatial division multiplexing enabled elastic optical networks （SDM-EONs） with multi-core fibers. First, the RCSA problem is modeled, and then a metric, i.e., CA spectrum compactness （CASC）, is designed to measure the spectrum status in SDM-EONs. Based on CASC, we propose two CA-RCSA algorithms, the first-fit （FF） CASC algorithm and the random-fit （RF） CASC algorithm. Simulation results show that our proposed algorithms can achieve better performance than the baseline algorithm in terms of blocking probability and spectrum utilization, with FF-CASC providing the best performance.

关键词： Blocking probability crosstalk Fiber optic networks Multiplexing Time division multiplexing

Dynamic glial response and crosstalk in demyelination-remyelination and neurodegeneration processes

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Neural Regeneration Research 2021年第7期16卷 1359-1368页

作者： Tianci Chu Lisa B.E.Shields Wenxin Zeng Yi Ping Zhang Yuanyi Wang Gregory N.Barnes Christopher B.Shields Jun Cai Pediatric Research Institute Department of PediatricsUniversity of Louisville School of MedicineLouisvilleKYUSA Norton Neuroscience Institute Norton HealthcareLouisvilleKYUSA Department of Spine Surgery The First Hospital of Jilin UniversityChangchunJilin ProvinceChina Department of Neurology University of Louisville School of MedicineLouisvilleKYUSA Department of Pharmacology and Toxicology University of LouisvilleLouisvilleKYUSA Department of Neurological Surgery University of Louisville School of MedicineLouisvilleKYUSA

Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin sheath in the central nervous system.It is characterized by blood-brain barrier dysfunction throughout the course of multiple sclerosis, followed by the entry of immune cells and activation of local microglia and astrocytes.Glial cells(microglia, astrocytes, and oligodendrocyte lineage cells) are known as the important mediators of neuroinflammation, all of which play major roles in the pathogenesis of multiple sclerosis.Network communications between glial cells affect the activities of oligodendrocyte lineage cells and influence the demyelination-remyelination process.A finely balanced glial response may create a favorable lesion environment for efficient remyelination and neuroregeneration.This review focuses on glial response and neurodegeneration based on the findings from multiple sclerosis and major rodent demyelination models.In particular, glial interaction and molecular crosstalk are discussed to provide insights into the potential cell-and molecule-specific therapeutic targets to improve remyelination and neuroregeneration.

关键词： astrocyte crosstalk demyelination glial response microglia/macrophage multiple sclerosis neurodegeneration neuroinflammation oligodendrocyte lineage cells remyelination

crosstalk between IL-15Rα^(+)tumor-associated macrophages and breast cancer cells reduces CD8+T cell recruitment

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Cancer Communications 2022年第6期42卷 536-557页

作者： Wenlong Zhang Qing Zhang Nanfei Yang Qian Shi Huifang Su Tingsheng Lin Zhonglei He Wenxin Wang Hongqian Guo Pingping Shen State Key Laboratory of Pharmaceutical Biotechnology and Department of Urology Nanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolSchool of Life SciencesNanjing UniversityNanjingJiangsu 210023P.R.China Department of Urology Drum Tower HospitalMedical School of Nanjing UniversityInstitute of UrologyNanjing UniversityNanjingJiangsu 210008P.R.China Shenzhen Research Institute of Nanjing University Shenzhen 518000China Department of Cellular and Integrative Physiology The University of Texas Health Science Center at San AntonioSan AntonioTexas 78229-3904USA Charles Institute of Dermatology School of MedicineUniversity College DublinDublin Eircode D04 V1W8Ireland

Background:Interleukin-15(IL-15)is a promising immunotherapeutic agent owing to its powerful immune-activating effects.However,the clinical benefits of these treatments are limited.crosstalk between tumor cells and immune cells plays an important role in immune escape and immunotherapy drug resistance.Herein,this study aimed to obtain in-depth understanding of crosstalk in the tumor microenvironment for providing potential therapeutic strategies to prevent tumor progression.Methods:T-cell killing assays and co-culture models were developed to determine the role of crosstalk between macrophages and tumor cells in breast cancer resistant to IL-15.Western blotting,histological analysis,CRISPR-Cas9 knockout,multi-parameter flow cytometry,and tumor cell-macrophage co-injection mouse models were developed to examine the mechanism by which IL-15Rα^(+)tumor-associated macrophages(TAMs)regulate breast cancer cell resistance to IL-15.Results:We found thatmacrophages contributed to the resistance of tumor cells to IL-15,and tumor cells induced macrophages to express high levels of theαsubunit of the IL-15 receptor(IL-15Rα).Further investigation showed that IL-15Rα^(+)TAMs reduced the protein levels of chemokine CX3C chemokine ligand 1(CX3CL1)in tumor cells to inhibit the recruitment of CD8^(+)T cells by releasing the IL-15/IL-15Rαcomplex(IL-15Rc).Administration of an IL-15Rc blocking peptide markedly suppressed breast tumor growth and overcame the resistance of cancer cells to anti-programmed cell death protein 1(PD-1)antibody immunotherapy.Interestingly,Granulocyte-macrophage colony-stimulating factor(GMCSF)inducedγchain(γc)expression to promote tumor cell-macrophage crosstalk,which facilitated tumor resistance to IL-15.Additionally,we observed that the non-transcriptional regulatory function of hypoxia inducible factor-1alpha(HIF-1α)was essential for IL-15Rc to regulateCX3CL1 expression in tumor cells.Conclusions:The IL-15Rc-HIF-1α-CX3CL1 signaling pathway serves as a crosstalk between macrophages and tumor cells in the t

关键词： breast cancer CD8^(+)T-cell crosstalk IL-15Rα immunotherapy tumor microenvironment tumor-associated macrophages

Parathyroid hormone increases alveolar bone homoeostasis during orthodontic tooth movement in rats with periodontitis via crosstalk between STAT3 and β-catenin

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International Journal of Oral Science 2020年第4期12卷 356-366页

作者： Cheng Zhang Tiancheng Li Chenchen Zhou Li Huang Yuyu Li Han Wang Peipei Duan Shujuan Zou Li Mei State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&Department of Orthodontics West China Hospital of StomatologySichuan UniversityChengduChina Discipline of Orthodontics Faculty of DentistryDepartment of Oral SciencesSir John Walsh Research InstituteUniversity of OtagoOtagoNew Zealand

Periodontitis patients are at risk of alveolar bone loss during orthodontic treatment.The aim of this study was to investigate whether intermittent parathyroid hormone(1–34)treatment(iPTH)could reduce alveolar bone loss during orthodontic tooth movement(OTM)in individuals with periodontitis and the underlying mechanism.A rat model of OTM in the context of periodontitis was established and alveolar bone loss was observed.The control,iPTH and iPTH+stattic groups received injections of vehicle,PTH and vehicle,or PTH and the signal transducer and activator of transcription 3(STAT3)inhibitor stattic,respectively.iPTH prevented alveolar bone loss by enhancing osteogenesis and suppressing bone resorption in the alveolar bone during OTM in rats with periodontitis.This effect of iPTH was along with STAT3 activation and reduced by a local injection of stattic.iPTH promoted osteoblastic differentiation and might further regulate the Wnt/β-catenin pathway in a STAT3-dependent manner.The findings of this study suggest that iPTH might reduce alveolar bone loss during OTM in rats with periodontitis through STAT3/β-catenin crosstalk.

关键词： STAT3 period crosstalk

Spatial distribution of IL4 controls iNKT cell-DC crosstalk in tumors

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Cellular & Molecular Immunology 2020年第5期17卷 496-506页

作者： Lu Wang Zhilan Liu Lili Wang Qielan Wu Xiang Li Di Xie Huimin Zhang Yongdeng Zhang Lusheng Gu Yanhong Xue Ting Yue Gang Liu Wei Ji Haiming Wei Tao Xu Li Bai Division of Life Sciences and Medicine Department of Oncology of The First Affiliated HospitalThe CAS Key Laboratory of Innate Immunity and Chronic DiseaseUniversity of Science and Technology of China230027 HefeiChina National Key Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of Sciences100101 BeijingChina School of Life Sciences University of Science and Technology of China230027 HefeiChina National Synchrotron Radiation Laboratory University of Science and Technology of China230027 HefeiChina

The spatiotemporal distribution of cytokines orchestrates immune responses in vivo,yet the underlying mechanisms remain to be explored.We showed here that the spatial distribution of interleukin-4(IL4)in invariant natural killer T(iNKT)cells regulated crosstalk between iNKT cells and dendritic cells(DCs)and controlled iNKT cell-mediated T-helper type 1(Th1)responses.The persistent polarization of IL4 induced by strong lipid antigens,that is,α-galactosylceramide(αGC),caused IL4 accumulation at the immunological synapse(IS),which promoted the activation of the IL4R-STAT6(signal transducer and activator of transcription 6)pathway and production of IL12 in DCs,which enhanced interferon-γ(IFNγ)production in iNKT cells.Conversely,the nonpolarized secretion of IL4 induced by Th2 lipid antigens with a short or unsaturated chain was incapable of enhancing this iNKT cell-DC crosstalk and thus shifted the immune response to a Th2-type response.The nonpolarized secretion of IL4 in response to Th2 lipid antigens was caused by the degradation of Cdc42 in iNKT cells.Moreover,reduced Cdc42 expression was observed in tumorinfiltrating iNKT cells,which impaired IL4 polarization and disturbed iNKT cell-DC crosstalk in tumors.

关键词： Spatial distribution Polarization IL4 iNKT DC crosstalk Tumor

The crosstalk between autophagy and ferroptosis:what can we learn to target drug resistance in cancer?

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Cancer Biology & Medicine 2019年第4期16卷 630-646页

作者： Yulu Zhou Yong Shen Cong Chen Xinbing Sui Jingjing Yang Linbo Wang Jichun Zhou Department of Surgical Oncology Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhou 310016China Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Provinee Hangzhou 310016China Department of Breast Surgery First Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310006China Department of Medical Oncology Holistic Integrative Oncology Institutes and Holistic Integrative Cancer Center of Traditional Chinese and Western MedicineThe Affiliated Hospital of Hangzhou Normal UniversityCollege of MedicineHangzhou Normal UniversityHangzhou 310012China Department of Cancer Pharmacology Holistic Integrative Pharmacy InstitutesCollege of MedicineHangzhou Normal UniversityHangzhou 310012China Key Laboratory of Elemene Class Anti-cancer Chinese Medicine of Zhejiang Provinee and Engineering Laboratory of Development and Application of Traditional Chinese Medicine from Zhejiang Provinee Hangzhou Normal UniversityHangzhou 310012China

Autophagy is a conserved intracellular degradation system that plays a dual role in cell death;thus,therapies targeting autophagy in cancer are somewhat controversial.Ferroptosis is a new form of regulated cell death featured with the iron-dependent accumulation of lethal lipid ROS.This pathway is morphologically,biochemically and genetically distinct from other forms of cell death.Accumulating studies have revealed crosstalk between autophagy and ferroptosis at the molecular level.In this review,we summarize the mechanisms of ferroptosis and autophagy,and more importantly,their roles in the drug resistance of cancer.Numerous connections between ferroptosis and autophagy have been revealed,and a strong causal relationship exists wherein one process controls the other and can be utilized as potential therapeutic targets for cancer.The elucidation of when and how to modulate their crosstalk using therapeutic strategies depends on an understanding of the fine-tuned switch between ferroptosis and autophagy,and approaches designed to manipulate the intensity of autophagy might be the key.

关键词： Autophagy ferroptosis crosstalk cancer drug resistance