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Mitochondrial Reactive Oxygen Species Elicit Acute and Chronic itch via Transient Receptor Potential Canonical 3 Activation in Mice

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Neuroscience Bulletin 2022年第4期38卷 373-385页

作者： Seong-Ah Kim Jun Ho Jang Wheedong Kim Pa Reum Lee Yong Ho Kim Hue Vang Kihwan Lee Seog Bae Oh Department of Neurobiology and Physiology School of Dentistry and Dental Research InstituteSeoul National UniversitySeoul 03080Republic of Korea Department of Brain and Cognitive Sciences College of Natural SciencesSeoul National UniversitySeoul 08826Republic of Korea Gachon Pain Center and Department of Physiology College of MedicineGachon UniversityIncheon 21999Republic of Korea Tooth-Periodontium Complex Medical Research Center School of DentistrySeoul National UniversitySeoul 03080Republic of Korea

Mitochondrial reactive oxygen species(mROS)that are overproduced by mitochondrial dysfunction are linked to pathological conditions including sensory abnormalities.Here,we explored whether mROS overproduction induces itch through transient receptor potential canonical 3(TRPC3),which is sensitive to ROS.Intradermal injection of antimycin A(AA),a selective inhibitor of mitochondrial electron transport chain complex III for mROS overproduction,produced robust scratching behavior in naïve mice,which was suppressed by MitoTEMPO,a mitochondria-selective ROS scavenger,and Pyr10,a TRPC3-specific blocker,but not by blockers of TRPA1 or TRPV1.AA activated subsets of trigeminal ganglion neurons and also induced inward currents,which were blocked by MitoTEMPO and Pyr10.Besides,dry skin-induced chronic scratching was relieved by MitoTEMPO and Pyr10,and also by resveratrol,an antioxidant.Taken together,our results suggest that mROS elicit itch through TRPC3,which may underlie chronic itch,representing a potential therapeutic target for chronic itch.

关键词： Mitochondria Reactive oxygen species TRPC3 itch Dry skin Trigeminal ganglia

TNF-αTNFR1 Signaling is Required for the Full Expression of Acute and Chronic itch in Mice via Peripheral and Central Mechanisms

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Neuroscience Bulletin 2018年第1期34卷 42-53页

作者： Xiuhua Miao Ya Huang Teng-Teng Liu Ran Guo Bing Wang Xue-Long Wang Li-Hua Chen Yan Zhou Ru-Rong Ji Tong Liu The Affiliated Zhangjiagang Hospital of Soochow University Zhangjiagang 215600 China Institute of Neuroscience Soochow University Suzhou 215021 China Capital Medical University Electric Power Teaching Hospital Beijing 100073 China Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases Department of Nutrition and Food Hygiene School of Public Health Soochow University Suzhou 215123 China Department of Anesthesiology Duke University Medical Center Durham NC 27710 USA Department of Neurobiology Duke University Medical Center Durham NC 27710 USA

Increasing evidence suggests that cytokines and chemokines play crucial roles in chronic itch. In the present study, we evaluated the roles of tumor necrosis factor-alpha （TNF-c0 and its receptors TNF receptor subtype-I （TNFR1） and TNFR2 in acute and chronic itch in mice. Compared to wild-type （WT） mice, TNFRl-knockout （TNFR1-KO） and TNFR1/R2 double-KO （DKO）, but not TNFR2-KO mice, exhibited reduced acute itch induced by compound 48/80 and chloroquine （CQ）. Application of the TNF-synthesis inhibitor thalidomide and the TNF-at antagonist etanercept dose-dependently suppressed acute itch. Intradermal injection of TNF-α was not sufficient to evoke scratching, but potentiated itch induced by compound 48/80, but not CQ. In addition, compound 48/80 induced TNF-α mRNA expression in the skin, while CQ induced its expression in the dorsal root ganglia （DRG） and spinal cord. Furthermore, chronic itch induced by dry skin was reduced by administration of thalidomide and etaner- cept and in TNFR1/R2 DKO mice. Dry skin induced TNF- expression in the skin, DRG, and spinal cord and TNFR1 expression only in the spinal cord. Thus, our findings suggest that TNF-c^-fNFR1 signaling is required for the full expression of acute and chronic itch via peripheral and central mechanisms, and targeting TNFR1 may be benefi- cial for chronic itch treatment.

关键词： itch Tumor necrosis factor Tumor necrosis factor receptor Spinal cord Central sensitization

Spinal Circuits Transmitting Mechanical Pain and itch

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Neuroscience Bulletin 2018年第1期34卷 186-193页

作者： Bo Duan Longzhen Cheng Qiufu Ma Department of Molecular Cellular and Developmental Biology University of Michigan Institute of Brain Science the State Key Laboratory of Medical Neurobiology and the Collaborative Innovation Center for Brain Science Fudan University Dana-Farber Cancer Institute and Department of Neurobiology Harvard Medical School

In 1905, Henry Head first suggested that trans- mission of pain-related protopathic information can be negatively modulated by inputs from afferents sensing innocuous touch and temperature. In 1965, Melzak and Wall proposed a more concrete gate control theory of pain that highlights the interaction between unmyelinated C fibers and myelinated A fibers in pain transmission. Here we review the current understanding of the spinal micro- circuits transmitting and gating mechanical pain or itch. We also discuss how disruption of the gate control could cause pain or itch evoked by innocuous mechanical stimuli, a hallmark symptom for many chronic pain or itch patients.

关键词： Pain itch Gate control Spinal cord

Descending Modulation of Spinal itch Transmission by Primary Somatosensory Cortex

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Neuroscience Bulletin 2021年第9期37卷 1345-1350页

作者： Zi-Han Wu Han-Yu Shao Yuan-Yuan Fu Xiao-Bo Wu De-Li Cao Sheng-Xiang Yan Wei-Lin Sha Yong-Jing Gao Zhi-Jun Zhang Department of Human Anatomy School of MedicineNantong UniversityNantong 226001China Institute of Pain Medicine Institute of Nautical MedicineNantong UniversityNantong 226019China Co-innovation Center of Neuroregeneration Nantong UniversityNantong 226001China

Dear Editor,itch(pruritus)is an unpleasant somatic sensation that is accompanied by the desire to scratch.While itch provides a warning signal that protects us from potential threats in normal conditions,severe or chronic itch associated with dermatosis or systemic diseases is often difficult to alleviate and causes severe skin and tissue damage.

关键词： sensation itch Spinal

Infection,Pain,and itch

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Neuroscience Bulletin 2018年第1期34卷 109-119页

作者： Isaac M.Chiu Department of Microbiology and Immunobiology Division of Immunology Harvard Medical School

Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future patho- gen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host- microbe interactions.

关键词： Pain itch Bacteria Pathogens Infection Inflammation Viruses

Immune regulation by protein ubiquitination: roles of the E3 ligases VHL and itch

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Protein & Cell 2019年第6期10卷 395-404页

作者： Daisuke Aki Qian Li Hui Li Yun-Cai Liu Jee Ho Lee Institute for Immunology Tsinghua-Peking Center for Life Sciences School of Medicine Tsinghua University Beijing 100084 China La Jolla Institute for Allergy and Immunology La Jolla CA 92037 USA

Protein ubiquitination is an important means of posttranslational modification which plays an essential role in the regulation of various aspects of leukocyte development and function. The specificity of ubiquitin tagging to a protein substrate is determined by E3 ubiquitin ligases via defined E3-substrate interactions. In this review, we will focus on two E3 ligases, VHL and itch, to discuss the latest progress in understanding their roles in the differentiation and function of CD4+ T helper cell subsets, the stability of regulatory T cells, effector function of CD8+ T cells, as well as the development and maturation of innate lymphoid cells. The biological implications of these E3 ubiquitin ligases will be highlighted in the context of normal and dysregulated immune responses including the control of homeostasis, inflammation, auto-immune responses and anti-tumor immunity. Further elucidation of the ubiquitin system in immune cells will help in the design of new therapeutic interventions for human immunological diseases and cancer.

关键词： ubiquitin E3ligase VHL HIF itch WWP2 Cbl-b inflammation autoimmunity

Spinal Mechanisms of itch Transmission

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Neuroscience Bulletin 2018年第1期34卷 156-164页

作者： Devin M.Barry Admire Munanairi Zhou-Feng Chen Center for the Study of itch Washington University School of Medicine Department of Anesthesiology Washington University School of Medicine Department of Psychiatry Washington University School of Medicine Developmental Biology Washington University School of Medicine

Peripheral itch stimuli are transmitted by sensory neurons to the spinal cord dorsal horn, which then transmits the information to the brain. The molecular and cellular mechanisms within the dorsal horn for itch transmission have only been investigated and identified during the past ten years. This review covers the progress that has been made in identifying the peptide families in sensory neurons and the receptor families in dorsal horn neurons as putative itch transmitters, with a focus on gastrin-releasing peptide （GRP）--GRP receptor signaling. Also discussed are the signaling mechanisms, including opioids, by which various types of itch are transmitted and modulated, as well as the many conflicting results arising from recent studies.

关键词： itch Neuropeptides Spinal cord DRG GPCR signaling

Regulation of Pain and itch by TRP Channels

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Neuroscience Bulletin 2018年第1期34卷 120-142页

作者： Carlene Moore Rupali Gupta Sven-Eric Jordt Yong Chen Wolfgang B.Liedtke Department of Neurology Duke University Medical Center Department of Anesthesiology Duke University Medical Center

Nociception is an important physiological process that detects harmful signals and results in pain perception. In this review, we discuss important experimental evidence involving some TRP ion channels as molecular sensors of chemical, thermal, and mechanical noxious stimuli to evoke the pain and itch sensations. Among them are the TRPA1 channel, members of the vanilloid subfamily （TRPV1, TRPV3, and TRPV4）, and finally members of the melastatin group （TRPM2, TRPM3, and TRPMS）. Given that pain and itch are pro-survival, evolutionarily-honed protective mechanisms, care has to be exercised when developing inhibitory/modulatory com- pounds targeting specific pain/itch-TRPs so that physio- logical protective mechanisms are not disabled to a degree that stimulus-mediated injury can occur. Such events have impeded the development of safe and effective TRPV1- modulating compounds and have diverted substantial resources. A beneficial outcome can be readily accom- plished via simple dosing strategies, and also by incorpo- rating medicinal chemistry design features during compound design and synthesis. Beyond clinical use, where compounds that target more than one channel might have a place and possibly have advantageous features, highly specific and high-potency compounds will be helpful in mechanistic discovery at the structure-function level.

关键词： TRP channels Pain itch Nociceptors - Inflammation Lipids Temperature Hyperalgesia Nerve damage Neuropathic pain Mechanotransduction Allodynia

Antioxidants Attenuate Acute and Chronic itch:Peripheral and Central Mechanisms of Oxidative Stress in Pruritus

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Neuroscience Bulletin 2017年第4期33卷 423-435页

作者： Feng-Ming Zhou Ruo-Xiao Cheng Shuai Wang Ya Huang Yong-Jing Gao Yan Zhou Teng-Teng Liu Xue-Long Wang Li-Hua Chen Tong Liu Department of Neurology The Second Affiliated Hospital of Soochow UniversitySuzhou 215004China Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases Department of Nutrition and Food HygieneSchool of Public HealthSoochow UniversitySuzhou 215123China Institute of Neuroscience Soochow UniversitySuzhou 215123China Institute of Nautical Medicine Nantong UniversityNantong 226001China Beijing Electric Power Hospital Beijing 100073China

itch（pruritus） is one of the most disabling syndromes in patients suffering from skin, liver, or kidney diseases. Our previous study highlighted a key role of oxidative stress in acute itch. Here, we evaluated the effects of antioxidants in mouse models of acute and chronic itch and explored the potential mechanisms. The effects of systemic administration of the antioxidants N-acetyl-Lcysteine（NAC） and N-tert-butyl-a-phenylnitrone（PBN）were determined by behavioral tests in mouse models of acute itch induced by compound 48/80 or chloroquine, and chronic itch by treatment with a mixture of acetonediethyl-ether-water. We found that systemic administration of NAC or PBN significantly alleviated compound 48/80-and chloroquine-induced acute itch in a dose-dependent manner, attenuated dry skin-induced chronic itch, and suppressed oxidative stress in the affected skin.Antioxidants significantly decreased the accumulation of intracellular reactive oxygen species directly induced by compound 48/80 and chloroquine in the cultured dorsal root ganglia-derived cell line ND7-23. Finally, the antioxidants remarkably inhibited the compound 48/80-induced phosphorylation of extracellular signal-regulated kinase in the spinal cord. These results indicated that oxidative stress plays a critical role in acute and chronic itch in the periphery and spinal cord and antioxidant treatment may be a promising strategy for anti-itch therapy.

关键词： Oxidative stress Antioxidants itch TRPA1 Extracellular signal-regulated kinase