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Neutrophils in chronic inflammatory diseases

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cellular & Molecular Immunology 2022年第2期19卷 177-191页

作者： Andrea Herrero-Cervera Oliver Soehnlein Ellinor Kenne Institute for Experimental Pathology Center for Molecular Biology of InflammationWestfälische Wilhelms-Universität MünsterMünsterGermany Department of Physiology and pharmacology Karolinska InstitutetStockholmSweden.

Chronic inflammation is a component of many disease conditions that affect a large group of individuals *** inflammation is characterized by persistent,low-grade inflammation and is increased in the aging *** are normally the first responders to acute inflammation and contribute to the resolution of ***,in chronic inflammation,the role of neutrophils is less well understood and has been described as either beneficial or detrimental,causing tissue damage and enhancing the immune *** evidence suggests that neutrophils are important players in several chronic diseases,such as atherosclerosis,diabetes mellitus,nonalcoholic fatty liver disease and autoimmune *** review will highlight the interaction of neutrophils with other cells in the context of chronic inflammation,the contribution of neutrophils to selected chronic inflammatory diseases,and possible future therapeutic strategies.

关键词： Chronic Inflammation Disease Neutrophil Neutrophil extracellular traps

Oxidative stress and diabetes:antioxidative strategies

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Frontiers of Medicine 2020年第5期14卷 583-600页

作者： Pengju Zhang Tao Li Xingyun Wu Edouard C.Nice Canhua Huang Yuanyuan Zhang Department of pharmacology West China School of Basic Medical Sciences&Forensic MedicineSichuan UniversityChengdu 610041China Department of Biochemistry and Molecular biology Monash UniversityClaytonVictoriaAustralia

Diabetes mellitus is one of the major public health problems *** recent evidence suggests that the cellular reduction-oxidation(redox)imbalance leads to oxidative stress and subsequent occurrence and development of diabetes and related complications by regulating certain signaling pathways involved in p-cell dysfunction and insulin *** oxide species(ROS)can also directly oxidize certain proteins(defined as redox modification)involved in the diabetes *** are a number of potential problems in the clinical application of antioxidant therapies including poor solubility,storage instability and nonselectivity of *** antioxidant delivery systems may overcome pharmacokinetic and stability problem and improve the selectivity of scavenging *** have therefore focused on the role of oxidative stress and antioxidative therapies in the pathogenesis of diabetes *** therapeutic interventions against ROS and downstream targets are now possible and provide important new insights into the treatment of diabetes.

关键词： diabetes oxidative stress redox modification antioxidative therapy novel antioxidant delivery

Regulation of antitumor immunity by inflammation-induced epigenetic alterations

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cellular & Molecular Immunology 2022年第1期19卷 59-66页

作者： Michael Karin Shabnam Shalapour Department of pharmacology School of MedicineUniversity of California San DiegoLa JollaCAUSA Laboratory of Gene Regulation and Signal Transduction Department of PharmacologySchool of MedicineUniversity of California San DiegoLa JollaCAUSA Department of Cancer biology University of Texas MD Anderson Cancer CenterHoustonTXUSA

Chronic inflammation promotes tumor development,progression,and metastatic dissemination and causes treatment *** accumulation of genetic alterations and loss of normal cellular regulatory processes are not only associated with cancer growth and progression but also result in the expression of tumor-specific and tumor-associated antigens that may activate antitumor *** antagonism between inflammation and immunity and the ability of cancer cells to avoid immune detection affect the course of cancer development and treatment *** inflammation,particularly acute inflammation,supports T-cell priming,activation,and infiltration into infected tissues,chronic inflammation is mostly ***,the main mechanisms that dictate the outcome of the inflammation-immunity interplay are not well *** data suggest that inflammation triggers epigenetic alterations in cancer cells and components of the tumor *** alterations can affect and modulate numerous aspects of cancer development,including tumor growth,the metabolic state,metastatic spread,immune escape,and immunosuppressive or immunosupportive leukocyte *** this review,we discuss the role of inflammation in initiating epigenetic alterations in immune cells,cancer-associated fibroblasts,and cancer cells and suggest how and when epigenetic interventions can be combined with immunotherapies to improve therapeutic outcomes.

关键词： Inflammation Epigenetics Antitumor immunity Immunotherapy

Sensitivity analysis for stochastic and deterministic models of nascent focal adhesion dynamics

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International Journal of Biomathematics 2017年第7期10卷 237-265页

作者： Hannah R. Biegel Alex Quackenbush Hannah Callender Highlander departments of Mathematics and biology University of Portland 5000 North Willamette Boulevard Portland Oregon 97203 USA Department of Mathematics University of Portland 5000 North Willamette Boulevard Portland Oregon 97203 USA

Sensitivity analysis （SA） is a critical part of modeling any biological system due to the inherent uncertainty in model output, as introduced by parameter values that have not been experimentally determined. SA therefore provides deeper understanding of the system by painting a picture of the extent to which certain model outputs vary in rela- tionship to changes in model parameters. Here we explore two types of global SA for recently developed models of nascent focal adhesion formation, a key step in cellular movement. While many SA methods have been used for deterministic methods, we uti- lize methods for both stochastic and deterministic models, providing a more complete description of the parameters to which the focal adhesion model is most sensitive. Spe- cific recommendations for further experimentation in the process of cellular motility are proposed in response to the SA.

关键词： Sensitivity analysis method of Morris FAST focal adhesion dynamics cel-lular motility stochastic models.

Current methods for the maturation of induced pluripotent stem cellderived cardiomyocytes

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World Journal of Stem Cells 2019年第1期11卷 33-43页

作者： Pranav Machiraju Steven C Greenway departments of Pediatrics and Cardiac Sciences Alberta Children’s Hospital Research Institute Libin Cardiovascular Institute of Alberta Cumming School of MedicineUniversity of Calgary departments of Pediatrics Cardiac Sciences Biochemistry & Molecular Biology Alberta Children’s Hospital Research Institute Libin Cardiovascular Institute of Alberta Cumming School of Medicine University of Calgary

Induced pluripotent stem cells(iPSCs) were first generated by Yamanaka and colleagues over a decade ago. Since then, iPSCs have been successfully differentiated into many distinct cell types, enabling tissue-, disease-, and patientspecific in vitro modelling. Cardiovascular disease is the greatest cause of mortality worldwide but encompasses rarer disorders of conduction and myocardial function for which a cellular model of study is ideal. Although methods to differentiate iPSCs into beating cardiomyocytes(iPSC-CMs) have recently been adequately optimized and commercialized, the resulting cells remain largely immature with regards to their structure and function,demonstrating fetal gene expression, disorganized morphology, reliance on predominantly glycolytic metabolism and contractile characteristics that differ from those of adult cardiomyocytes. As such, disease modelling using iPSC-CMs may be inaccurate and of limited utility. However, this limitation is widely recognized, and numerous groups have made substantial progress in addressing this problem. This review highlights successful methods that have been developed for the maturation of human iPSC-CMs using small molecules,environmental manipulation and 3-dimensional(3 D) growth approaches.

关键词： Induced pluripotent stem cells Induced pluripotent stem cell-derived cardiomyocytes Regenerative medicine Stem cell biology Translational research

Chaperone-mediated autophagy: roles in neurodegeneration

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Translational Neurodegeneration 2014年第1期3卷 141-147页

作者： Gang Wang Zixu Mao departments of pharmacology and Neurology Emory University School of MedicineAtlantaGA 30322USA Center for Neurodegenerative Diseases Emory University School of MedicineAtlantaGA 30322USA

Chaperone-mediated autophagy(CMA)selectively delivers cytosolic proteins with an exposed CMA-targeting motif to lysosomes for degradation and plays an important role in protein quality control and cellular homeostasis.A growing body of evidence supports the hypothesis that CMA dysfunction may be involved in the pathogenic process of neurodegenerative *** down-regulation and compensatory up-regulation in CMA activities have been observed in association with neurodegenerative *** studies have revealed several new mechanisms by which CMA function may be involved in the regulation of factors critical for neuronal viability and ***,we summarize these recent advances in the understanding of the relationship between CMA dysfunction and neurodegeneration and discuss the therapeutic potential of targeting CMA in the treatment of neurodegenerative diseases.

关键词： Chaperone-mediated autophagy Protein posttranslational modifications Neurodegeneration,Alzheimer’s disease Parkinson’s disease

Pharmacological strategies for treating misfolded rhodopsinassociated autosomal dominant retinitis pigmentosa

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Neural Regeneration Research 2022年第1期17卷 110-112页

作者： Yibo Xi Yuanyuan Chen Department of Ophthalmology University of PittsburghPittsburghPAUSA Department of pharmacology and Chemical biology University of PittsburghPittsburghPAUSA McGowan Institute of Regenerative Medicine University of PittsburghPittsburghPAUSA

Mutations that cause protein misfolding are implicated in conditions such as retinitis pigmentosa(RP),Usher Syndrome,and myocilin associated primary open angle *** aggregation and continuous degradation of a highly abundant misfolded protein add proteolytic load of the affected *** subtle balance of cellular homeostasis,once disrupted by an overwhelmed proteolytic system,will lead to cell death and tissue degeneration.

关键词： retinitis degeneration homeostasis

Pathway-selective suppression of chemokine receptor signaling in B cells by LPS through downregulation of PLC-b2

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cellular & Molecular Immunology 2010年第6期7卷 428-439页

作者： Aiko-Konno Shirakawa Fang Liao Hongwei H Zhang Michael N Hedrick Satya P Singh Dianqing Wu Joshua M Farber Inflammation biology Section Laboratory of Molecular ImmunologyNational Institute of Allergy and Infectious DiseasesNational Institutes of HealthBethesdaMDUSA Department of pharmacology Yale University School of MedicineNew HavenCTUSA

Lymphocyte activation leads to changes in chemokine receptor *** are limited data,however,on how lymphocyte activators can alter chemokine signaling by affecting downstream *** hypothesized that B cell-activating agents might alter chemokine responses by affecting downstream signal transducers,and that such effects might differ depending on the *** found that activating mouse B cells using either anti-IgM or lipopolysaccharide(LPS)increased the surface expression of CCR6 and CCR7 with large increases in chemotaxis to their cognate *** contrast,while anti-IgM also led to enhanced calcium responses,LPS-treated cells showed only small changes in calcium signaling as compared with cells that were freshly *** particular interest,we found that LPS caused a reduction in the level of B-cell phospholipase C(PLC)-b2 mRNA and *** obtained using PLC-b22/2 mice showed that the b2 isoform mediates close to one-half the chemokine-induced calcium signal in resting and anti-IgM-activated B cells,and we found that calcium signals in the LPS-treated cells were boosted by increasing the level of PLC-b2 using transfection,consistent with a functional effect of downregulating ***,our results show activator-specific effects on responses through B-cell chemokine receptors that are mediated by quantitative changes in a downstream signal-transducing protein,revealing an activity for LPS as a downregulator of PLC-b2,and a novel mechanism for controlling chemokine-induced signals in lymphocytes.

关键词： B cells calcium chemokine chemotaxis GPCR

Blockade of Na^+/H^+ exchanger type 3 causes intracellular acidification and hyperexcitability via inhibition of pH-sensitive K^+ channels in chemosensitive respiratory neurons of the dorsal vagal nucleus in rats

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Neuroscience Bulletin 2014年第1期30卷 43-52页

作者： Jing Zhang Hui Peng Sigrid C.Veasey Jing Ma Guang-Fa Wang Ke-Wei Wang Department of Respiratory and Critical Care Medicine Peking University First Hospital departments of Neurobiology and Molecular and cellular pharmacology Peking University Health Science Center Center for Sleep and Circadian Neurobiology University of Pennsylvania School of Medicine Department of Medicine University of Pennsylvania School of Medicine

Extracellular pH （pHe） and intracellular pH （pHi） are important factors for the excitability of chemosensitive central respiratory neurons that play an important role in respiration and obstructive sleep apnea. It has been proposed that inhibition of central Na^＋/ H^＋ exchanger 3 （NHE-3）, a key pHi regulator in the brainstem, decreases the pH, leading to membrane depolarization for the maintenance of respiration. However, how intracellular pH affects the neuronal excitability of respiratory neurons remains largely unknown. In this study, we showed that NHE-3 mRNA is widely distributed in respiration-related neurons of the rat brainstem, including the dorsal vagal nucleus （DVN）. Whole-cell patch clamp recordings from DVN neurons in brain slices revealed that the standing outward current （Iso） through pH-sensitive K^＋ channels was inhibited in the presence of the specific NHE-3 inhibitor AVE0657 that decreased the pHi. Exposure of DVN neurons to an acidified PIle and AVE0657 （5 μmol/L） resulted in a stronger effect on firing rate and Iso than acidified pHe alone. Taken together, our results showed that intracellular acidification by blocking NHE-3 results in inhibition of a pH- sensitive K^＋ current, leading to synergistic excitation of chemosensitive DVN neurons for the regulation of respiration.

关键词： Na^+/H^+ exchange potassium channel dorsal vagal nucleus in situ hybridization respiration