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The role of purinergic receptors in neural repair and regeneration after spinal cord injury

Neural Regeneration Research 2023年第8期18卷 1684-1690页

作者： Rui-Dong Cheng Wen Ren Ben-Yan Luo Xiang-Ming Ye Center for Rehabilitation Medicine Rehabilitation&Sports Medicine Research Institute of Zhejiang ProvinceDepartment of Rehabilitation MedicineZhejiang Provincial People’s Hospital(Affiliated People’s HospitalHangzhou Medical College)HangzhouZhejiang ProvinceChina Department of Family Medicine The First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang ProvinceChina Department of Neurology&Brain Medical Center The First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang ProvinceChina

Spinal cord injury is a serious injury of the central nervous system that results in neurological *** pathophysiological mechanisms underlying spinal cord injury,as well as the mechanisms involved in neural repair and regeneration,are highly *** there have been many studies on these mechanisms,there is no effective intervention for such *** spinal cord injury,neural repair and regeneration is an important part of improving neurological function after injury,although the low regenerative ability of nerve cells and the difficulty in axonal and myelin regeneration after spinal cord injury hamper functional *** amounts of ATP and its metabolites are released after spinal cord injury and participate in various aspects of functional regulation by acting on purinergic receptors which are widely expressed in the spinal *** processes mediate intracellular and extracellular signalling pathways to improve neural repair and regeneration after spinal cord *** article reviews research on the mechanistic roles of purinergic receptors in spinal cord injury,highlighting the potential role of purinergic receptors as interventional targets for neural repair and regeneration after spinal cord injury.

关键词： glial cells glial scar inflammatory responses neural regeneration neural repair neural stem cells purinergic receptors spinal cord injury

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Adrenergic signaling mediates pancreatic hyperalgesia through activation of purinergic receptors in primary sensory neurons in a rat model of chronic pancreatitis

Adrenergic signaling mediates pancreatic hyperalgesia throug...

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中国神经科学学会第十届全国学术会议

作者： Hong-Yan ZHU Chun-Hua ZHANG Shu-Fen HU Guang-Yin XU Institute of Neuroscience Key Laboratory of Pain Basic Research and Clinic TherapyDepartment of NeurobiologySoochow University

Objective The neurobiologic basis of pancreatic hyperalgesia in chronic pancreatitis（CP） is poorly understood and there is a great need to identify novel therapeutic *** aim of this study was designed to investigate roles of norepinephrine（NE） and P2X receptor signaling pathways in the pathogenesis of pancreatic pain in a rat model of *** CP was induced in adult rats by intraductal injection of trinitrobenzene sulfonic acid（TNBS）.DiI dye injected into pancreas was used to label pancreas innervating dorsal root ganglion（DRG） neurons.P2X receptor-mediated responses in pancreas-specific DRG neurons were measured using calcium imaging *** blot analysis was performed to examine protein *** hyperalgesia was assessed by nocifensive behavior to mechanical stimulation of rat *** TNBS-injected rats exhibited a robotic pancreatic pain,which was associated with a 2-fold increase in ATP-induced calcium signals when compared with age-matched controls（P＜0.05）.TNBS injection also significantly increased expression of adrenergic β-receptors in thoracic *** administration of P2X receptor antagonist suramine or β receptor antagonist propranolol markedly reduced referred somatic hyperalgesia in rats with ***,these two antagonists failed to produce analgesic effect in healthy control *** addition,incubation of norepinephrine（NE） significantly enhanced ATP-induced calcium signal,which was abolished by propranolol but not by adrenergic a-receptor antagonist *** potentiation of ATP response induced by NE incubation was partially blocked by protein kinase A inhibitor ***,an adenylyl cyclase activator,markedly enhanced ATP-induced responses of pancreas specific DRG *** Sensitization of P2X receptors,which was likely mediated by adrenergic signaling in primary sensory neurons,contributes to pancreatic hyperalgesia,thus identifying a potential target for treating pancreatic

关键词： chronic pancreatitis norepinephrine dorsal root ganglion calcium image purinergic receptors protein kinase A

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purinergic contraction of the rat vas deferens in L-NAME-induced hypertension：effect of sildenafil

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Asian Journal of Andrology 2010年第3期12卷 415-421,I0012页

作者： Serap Gur Suresh C. Sikka Gillian E. Knight Geoffrey Bumstock Wayne J.G. Hellstrom Department of Urology Tulane University Health Sciences Center New Orleans LA 70112 USA Autonomic Neuroscience Centre Royal Free and University College Medical School Rowland Hill Street London NW32PF UK

Hypertension （HTN） is a risk factor for erectile dysfunction, but its effect on vas deferens （VD） contractility and the ejaculatory response has not been delineated. NG-nitro-L-arginine methyl ester （L-NAME）, a nitric oxide synthase inhibitor, was used for induction of nitric oxide （NO）-deficient HTN. Our aim was to evaluate the effects of L-NAME-induced HTN on rat VD contractility and to determine whether sildenafil affects VD contractility. A total of 36 male rats were divided into （1） control, （2）L-NAME-HTN, （3） sildenafil treated L-NAME-HTN groups. Group 2 was treated with L-NAME （40 mg kgI per day） in drinking water for 4 weeks. Group 3 received sildenafil （1.5 mg kg^-1 per day, by oral gavage） concomitantly with L-NAME. The prostatic portion of the VD was subjected to electrical field stimulation （EFS, 1-20 Hz）, and the P2X1 agonist α,β-methylene ATP （α,β meATP, 100 μmol L^-1-1 μmol L-1） and the al-adrenoceptor agonist phenylephrine （Phe, 100 μmol L^-1-1 mmol L^-1） were used to construct concentration-response curves. These experiments were repeated in the presence of P2X receptor antagonist, pyridoxalphosphate-6-azophenyl-2＇,4＇-disulfonic acid （PPADS, 30 μmol L-1）. VD contractions in response to EFS, a,β-meATP and Phe were significantly enhanced by L-NAME. Sildenafil treatment in the L-NAME group improved the contractile response of VD to EFS （20 Hz）. In the presence of PPADS, the enhanced contractile response of VD to EFS and a,β-meATP in hypertensive rats was reversed. In the rat model of chronic NO depletion, the purinergic and adrenergic components and EFS affect VD contractility. The VD contractile response may be mediated more by the purinergic system than the adrenergic system, and sildenafil may alter the ejaculatory response in men with PE.

关键词： hypertensive rat NG-nitro-L-arginine methyl ester purinergic receptors P2X sildenafil vas deferens

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Adrenergic signaling mediates pancreatic hyperalgesia through activation ofpurinergic receptors in primary sensory neurons in rats with chronic pancreatitis

Adrenergic signaling mediates pancreatic hyperalgesia throug...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：徐广银朱宏岩周友浪周媛袁波张春华胡淑芬张弘弘苏州大学神经科学研究所江苏省重大神经精神疾病诊疗技术研究重点实验室苏州市疼痛研究与临床治疗重点实验室

Objective:The mechanism of pain in chronic pancreatitis（CP）is poorly understood and its treatment remains difficult,in large part due to our lack of knowledge about the neurobiological mechanisms in *** aim of this study was designed to investigate roles of norepinephrine（NE）and P2X receptor signaling pathway in the pathogenesis of pancreatic pain in a rat model of ***:CP was induced in male adult rats by intraductal injection of trinitrobenzene sulfonic acid（TNBS）.Pancreatic hyperalgesia was assessed by referred somatic behaviors to mechanical stimulation of rat *** I dye injected into pancreas was used to label pancreas innervating dorsal root ganglion（DRG）neurons.P2X receptor-mediated responses in pancreas DRG neurons were measured using calcium-imaging and whole cell patch clamp recording *** blot and PCR analysis was performed to examine protein and m RNA *** was performed to examine concentration of ***:Administration of purinergic receptor antagonist suramine or A317491attenuated pancreatic pain,in a dose-and time-dependent manner,in CP *** of P2X3 receptors and the ATP-induced current density of pancreas innervating thoracic DRG neurons were markedly enhanced after TNBS *** sensitization of P2X3 receptors?was reversed byβadrenergic receptor antagonist propranolol but not by adrenergic receptor antagonist *** was associated with an upregulation of expression ofβ2 adrenergic receptors in *** NE concentration in DRGs and pancreas was significantly enhanced in TNBS-treated *** injection also produced a 2-fold increase in ATP-induced calcium signals and amplified the NE-induced potentiation of ATP responses when compared with *** triple labeling techniques,we showed thatβ2 adrenergic receptors were colocalized with P2X3 receptors in pancreatic DRG ***,incubation of DRG neurons with NE significantly enhanced ATP-induced i

关键词： Chronic pancreatitis Dorsal root ganglion purinergic receptors Norepinephrine Protein kinase A

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The mechanisms of nucleotide actions in insulin resistance

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Journal of Genetics and Genomics 2022年第4期49卷 299-307页

作者： Kunpeng Liu Xiaogao Jin Xiaoying Zhang Hongkai Lian Jianping Ye Metabolic Disease Research Center Zhengzhou University Affiliated Zhengzhou Central HospitalZhengzhouHenan 450007China Cell-gene Therapy Translational Medicine Research Center The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Center for Advanced Medicine College of MedicineZhengzhou UniversityZhengzhouHenan 450007China Department of Orthopedics Zhengzhou Central HospitalZhengzhouHenan 450000China

Insulin resistance contributes to metabolic disorders in obesity and type 2 *** mechanisms of insulin resistance,the roles of glucose,fatty acids,and amino acids have been extensively documented in ***,the activities of nucleotides remain to be reviewed comprehensively in the regulation of insulin *** are well known for their activities in biosynthesis of DNA and RNA as well as their signaling activities in the form of c AMP and c *** activities in insulin resistance are dependent on the derivatives and corresponding *** and NADH,derivatives of adenosine,inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1,***,ADP and AMP,the well-known energy carriers,regulate cellular responses to insulin outside cells through the purinergic receptors in cell *** evidence suggests that ATP,NADH,c GAMP,and uridine are potential biomarkers of insulin ***,GTP and c GMP are likely the markers of insulin ***,studies crossing the biomedical fields are reviewed to characterize nucleotide activities in the regulation of insulin *** knowledge brings new insights into the mechanisms of insulin resistance.

关键词： Insulin resistance Nucleotide Adenosine Guanosine Uridine AMPK purinergic receptors

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Extracellular ADP facilitates monocyte recruitment in bacterial infection via ERK signaling

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Cellular & Molecular Immunology 2018年第1期15卷 58-73页

作者： Xiaoyu Zhang Juliang Qin Junyan Zou Zhangsheng Lv Binghe Tan Jueping Shi Yihan Zhao Hua Ren Mingyao Liu Min Qian Bing Du Shanghai Key Laboratory of Regulatory Biology Institute of Biomedical Sciences and School of Life SciencesEast China Normal UniversityShanghaiChina

As the most prominent clinical drug targets for the inhibition of platelet aggregation, P2Y12 and P2Y13 have been found to be highly expressed in both platelets and macrophages. However, the roles and function of P2Y12/13 in the regulation of macrophage-mediated innate immune responses remain unclear. Here, we demonstrate that adenosine 5′-diphosphate (ADP), the endogenous ligand of P2Y1, P2Y12 and P2Y13, was released both in E. coli-infected mice and from macrophages treated with either lipopolysaccharide (LPS) or Pam3CSK4. Furthermore, the expression of P2Y13 was clearly increased in both LPS-treated macrophages and tuberculosis patients. ADP protected mice from E. coli 0111-induced peritonitis by recruiting more macrophages to the infected sites. Consistent with this, ADP and ADP-treated cell culture medium attracted more macrophages in the transwell assay by enhancing the expression of MCP-1. Nevertheless, P2Y1 is dispensable for ADP-mediated protection against bacterial infection. However, either P2Y12/P2Y13 deficiency or blocking the downstream signaling of P2Y12/P2Y13 blocked the ADP-mediated immune response and allowed more bacteria to persist in the infected mice. Furthermore, extracellular signal-regulated kinase (ERK) phosphorylation was clearly increased by ADP, and this type of activation could be blocked by either forskolin or analogs of cyclic AMP (cAMP) (for example, 8-bromo-cAMP). Accordingly, ADP-induced MCP-1 production and protection against bacterial infection could also be reduced by U0126, forskolin and 8-bromo-cAMP. Overall, our study reveals a relationship between danger signals and innate immune responses, which suggests the potential therapeutic significance of ADP-mediated purinergic signaling in infectious diseases.

关键词： ADP cAMP danger signal MCP-1 purinergic receptors

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Changes in P2Y purinoreceptor-mediated intracellular calcium signal pathways results in inositol-1, 4, 5-triphosphate-sensitive calcium stores in rat small trigeminal ganglion neurons

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Neural Regeneration Research 2010年第12期5卷 906-910页

作者： Yuanyin Wang Andong Liu Jie Lei Min Xie Zhongwen Li Liecheng Wang Stomatological Hospital Anhui Medical University Hefei 230032 Anhui Province China Department of Physiiology School of Basic Medical Science Anhui Medical University Hefei 230032 Anhui Province China

BACKGROUND： Most of the currently available information on purinergic receptors （P2Rs） involved in pain transmission is based on results obtained in dorsal root ganglion or the spinal cord. However, the mechanism of P2Rs in trigeminal neuralgia remains unclear. OBJECTIVE： To investigate changes in the P2R-mediated calcium signaling pathway in nociceptive trigemJnal ganglion neurons. DESIGN, TIME AND SETTING： In vitro experiments were conducted at the Patch-Clamp Laboratory of Comprehensive Experiment Center of Anhui Medical University, China from September 2008 to June 2009. MATERIALS： Thapsigargin, caffeine, suramin, and adenosine 5＇-triphosphate were purchased from Sigma, USA. METHODS： Using Fura-2-based microfluorimetry, intracellular calcium concentration （[Ca^2＋]i） was measured in freshly isolated adult rat small trigeminal ganglion neurons before and after drug application. MAIN OUTCOME MEASURES： Fluorescent intensities were expressed as the ratio F340/F380 to observe [Ca^2＋]i changes. RESULTS： In normal extracellular solution and Ca^2＋-free solution, application of thapsigargin （1 μmol/L）, a sarcoplasmic reticulum Ca^2＋ pump adenosine 5＇-triphosphate inhibitor, as well as caffeine （20 mmol/L）, a ryanodine receptor agonist, triggered [Ca^2＋]i increase in small trigeminal ganglion neurons. A similar response was induced by application of adenosine 5＇-triphosphate （100 μmol/L）. In Ca^2＋-free conditions, adenosine 5＇-triphosphate-induced [Ca^2＋]i transients in small trigeminal ganglion neurons were inhibited in cells pre-treated with thapsigargin （P 〈 0.01）, but not by caffeine （P 〉 0.05）. In normal, extracellular solution, adenosine 5＇-triphosphate-induced [Ca^2＋]i transients in small trigeminal ganglion neurons were partly inhibited in cells pre-treated with thapsigargin （P 〈 0.05）. CONCLUSION： Inositol-1,4, 5-triphosphate （IP3）- and ryanodine-sensitive Ca^2＋ stores exist in rat nociceptive trigeminal ganglion neurons. Two pathways are involved in the purinorec

关键词： calcium stores cytoplasmic calcium trigeminal ganglion adenosine 5'-triphosphate purinergic receptors neurotrophic factor trigeminal neuralgia neural regeneration

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