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C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 pathway as a therapeutic target and regulatory mechanism for spinal cord injury
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作者 Xiangzi Wang Xiaofei Niu +4 位作者 Yingkai Wang Yang Liu Cheng Yang Xuyi Chen Zhongquan Qi 《Neural Regeneration Research》 SCIE CAS 2025年第8期2231-2244,共14页
Spinal cord injury involves non-reversible damage to the central nervous system that is characterized by limited regenerative capacity and secondary inflammatory damage.The expression of the C-C motif chemokine ligand... Spinal cord injury involves non-reversible damage to the central nervous system that is characterized by limited regenerative capacity and secondary inflammatory damage.The expression of the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis exhibits significant differences before and after injury.Recent studies have revealed that the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis is closely associated with secondary inflammatory responses and the recruitment of immune cells following spinal cord injury,suggesting that this axis is a novel target and regulatory control point for treatment.This review comprehensively examines the therapeutic strategies targeting the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis,along with the regenerative and repair mechanisms linking the axis to spinal cord injury.Additionally,we summarize the upstream and downstream inflammatory signaling pathways associated with spinal cord injury and the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis.This review primarily elaborates on therapeutic strategies that target the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis and the latest progress of research on antagonistic drugs,along with the approaches used to exploit new therapeutic targets within the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis and the development of targeted drugs.Nevertheless,there are presently no clinical studies relating to spinal cord injury that are focusing on the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis.This review aims to provide new ideas and therapeutic strategies for the future treatment of spinal cord injury. 展开更多
关键词 apoptosis c-c motif chemokine ligand 2/c-c motif chemokine receptor 2 pathway c-c motif chemokine receptor 2 antagonists chemokine ligand 2 chemokine receptor 2 inflammation macrophage microglia spinal cord injury therapeutic method
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The secondary injury cascade after spinal cord injury:an analysis of local cytokine/chemokine regulation 被引量:1
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作者 Daniel J.Hellenbrand Charles M.Quinn +8 位作者 Zachariah J.Piper Ryan T.Elder Raveena R.Mishra Taylor L.Marti Phoebe M.Omuro Rylie M.Roddick Jae Sung Lee William L.Murphy Amgad S.Hanna 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第6期1308-1317,共10页
After spinal cord injury,there is an extensive infiltration of immune cells,which exacerbates the injury and leads to further neural degeneration.Therefore,a major aim of current research involves targeting the immune... After spinal cord injury,there is an extensive infiltration of immune cells,which exacerbates the injury and leads to further neural degeneration.Therefore,a major aim of current research involves targeting the immune response as a treatment for spinal cord injury.Although much research has been performed analyzing the complex inflammatory process following spinal cord injury,there remain major discrepancies within previous literature regarding the timeline of local cytokine regulation.The objectives of this study were to establish an overview of the timeline of cytokine regulation for 2 weeks after spinal cord injury,identify sexual dimorphisms in terms of cytokine levels,and determine local cytokines that significantly change based on the severity of spinal cord injury.Rats were inflicted with either a mild contusion,moderate contusion,severe contusion,or complete transection,7 mm of spinal cord centered on the injury was harvested at varying times post-injury,and tissue homogenates were analyzed with a Cytokine/Chemokine 27-Plex assay.Results demonstrated pro-inflammatory cytokines including tumor necrosis factorα,interleukin-1β,and interleukin-6 were all upregulated after spinal cord injury,but returned to uninjured levels within approximately 24 hours post-injury,while chemokines including monocyte chemoattractant protein-1 remained upregulated for days post-injury.In contrast,several anti-inflammatory cytokines and growth factors including interleukin-10 and vascular endothelial growth factor were downregulated by 7 days post-injury.After spinal cord injury,tissue inhibitor of metalloproteinase-1,which specifically affects astrocytes involved in glial scar development,increased more than all other cytokines tested,reaching 26.9-fold higher than uninjured rats.After a mild injury,11 cytokines demonstrated sexual dimorphisms;however,after a severe contusion only leptin levels were different between female and male rats.In conclusion,pro-inflammatory cytokines initiate the inflammatory process and return to baseline within hours post-injury,chemokines continue to recruit immune cells for days post-injury,while anti-inflammatory cytokines are downregulated by a week post-injury,and sexual dimorphisms observed after mild injury subsided with more severe injuries.Results from this work define critical chemokines that influence immune cell infiltration and important cytokines involved in glial scar development after spinal cord injury,which are essential for researchers developing treatments targeting secondary damage after spinal cord injury. 展开更多
关键词 ASTROCYTES chemokineS cytokines inflammation macrophages MICROGLIA secondary damage spinal cord injury
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Mental disorders after myocardial infarction:potential mediator role for chemokines in heart-brain interaction?
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作者 Parth Patel Feiyan Yang +1 位作者 Dumitru A.Iacobas Lei Xi 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2024年第9期913-926,共14页
Acute myocardial infarction(MI)remains one of the leading causes of mortality and morbidity in the global communities.A prevailing topic that has attracted increasing attentions over the past few decades is the so-cal... Acute myocardial infarction(MI)remains one of the leading causes of mortality and morbidity in the global communities.A prevailing topic that has attracted increasing attentions over the past few decades is the so-called heart-brain interaction,in particular following a major traumatic event such as MI.Increased prevalence of depression and other mental disorders has been recognized in cardiac patients after MI,coronary catheterization,or cardiothoracic surgeries.In this review,we focus on the potential pathogenic mechanisms and pre-clinical transcriptomic evidence for identifying potential mediators of post-MI depression.We first summarize the conventional mechanistic understanding that leads to the current clinical management of post-MI depression with the use of selective serotonin reuptake inhibitors(SSRIs)and cognitive behavior and exercise therapies.We further envisage a possible role played by certain chemokines,e.g.,Chemokine(C-X-C motif)ligand 12(CXCL12)and Chemokine(C-C motif)ligand 2(CCL22),in serving as signaling molecules to connect the MI-induced heart damage to the pro-depressive changes in brain during the post-MI period.Future in-depth investigations into this chemokine hypothesis will be instrumental in developing new chemokine-targeted therapies for better management of the cardiac patients suffering from post-MI depression. 展开更多
关键词 chemokine DISORDERS POTENTIAL
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C-C趋化因子受体2阳性外泌体抑制单核细胞浸润改善缺血再灌注后心肌损伤的实验研究 被引量:2
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作者 李岩 刘凤菊 +1 位作者 李曦 尹娜 《中国医药》 2024年第5期689-693,共5页
目的探讨C-C趋化因子受体2阳性(CCR2^(+))外泌体调控小鼠心肌缺血再灌注(IR)损伤的作用机制。方法将12只C57小鼠完全随机分为野生型(WT)假手术组、WT手术(IR模型)组、CCR2-外泌体手术组和CCR2^(+)外泌体手术组,其中后3组均构建了心肌IR... 目的探讨C-C趋化因子受体2阳性(CCR2^(+))外泌体调控小鼠心肌缺血再灌注(IR)损伤的作用机制。方法将12只C57小鼠完全随机分为野生型(WT)假手术组、WT手术(IR模型)组、CCR2-外泌体手术组和CCR2^(+)外泌体手术组,其中后3组均构建了心肌IR损伤模型并给予相应处理。超声检测心脏结构及功能;Masson三色特殊染色法检测心脏组织内胶原沉积;转移酶介导的脱氧尿苷三磷酸缺口末端标记法检测心肌细胞凋亡;免疫组织化学染色及实时荧光定量聚合酶链反应法检测单核细胞招募相关C-C趋化因子配体2(CCL2)表达以及单核细胞表面CCR2表达;流式细胞术检测心肌IR后梗死部位淋巴细胞抗原6复合体C(Ly6C)和CD_(43)单核细胞数量。结果心肌IR手术后7 d,CCR2^(+)外泌体手术组小鼠心脏纤维化面积小于IR模型组[(16.8±8.1)%比(45.7±3.8)%];射血分数明显低于WT假手术组,但高于IR模型组;小鼠心肌细胞凋亡数量小于IR模型组;小鼠心脏中CCR2蛋白相对表达量小于IR模型组;小鼠再灌注区域CCR2阳性细胞面积小于IR模型组;小鼠再灌注部位Ly6C+的单核细胞数明显低于IR模型组,CD_(43)^(+)的单核细胞数明显高于IR模型组;小鼠心脏中CCL2 mRNA和蛋白相对表达量小于IR模型组(均P<0.05)。结论CCR2^(+)外泌体表现出明显的抗心肌IR损伤的作用,其机制是CCL2表达减少抑制单核细胞浸润,从而减轻了心肌损伤和抑制心力衰竭。 展开更多
关键词 缺血再灌注损伤 c-c趋化因子受体2 单核细胞 炎症 心肌梗死
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Macrophage migration inhibitory factor facilitates astrocytic production of the CCL2 chemokine following spinal cord injury 被引量:1
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作者 Han Zhang Yu-Ming Hu +6 位作者 Ying-Jie Wang Yue Zhou Zhen-Jie Zhu Min-Hao Chen Yong-Jun Wang Hua Xu You-Hua Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第8期1802-1808,共7页
Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation.Overproduced chemokines are responsible for the migratory process of the leukoc... Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation.Overproduced chemokines are responsible for the migratory process of the leukocytes,but the regulatory mechanism underlying the production of chemokines from resident cells of the spinal cord has not been fully elucidated.We examined the protein levels of macrophage migration inhibitory factor and chemokine C-C motif chemokine ligand 2 in a spinal cord contusion model at different time points following spinal cord injury.The elevation of macrophage migration inhibitory factor at the lesion site coincided with the increase of chemokine C-C motif chemokine ligand 2 abundance in astrocytes.Stimulation of primary cultured astrocytes with different concentrations of macrophage migration inhibitory factor recombinant protein induced chemokine C-C motif chemokine ligand 2 production from the cells,and the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine attenuated the stimulatory effect.Further investigation into the underlying mechanism on macrophage migration inhibitory factor-mediated astrocytic production of chemokine C-C motif chemokine ligand 2 revealed that macrophage migration inhibitory factor activated intracellular JNK signaling through binding with CD74 receptor.Administration of the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine following spinal cord injury resulted in the reduction of chemokine C-C motif chemokine ligand 2-recruited microglia/macrophages at the lesion site and remarkably improved the hindlimb locomotor function of rats.Our results have provided insights into the functions of astrocyte-activated chemokines in the recruitment of leukocytes and may be beneficial to develop interventions targeting chemokine C-C motif chemokine ligand 2 for neuroinflammation after spinal cord injury. 展开更多
关键词 ASTROCYTES CD74 chemokine chemokine c-c motif chemokine ligand 2(CCL2) cytokine inflammation LEUKOCYTE MAPKS migration inhibitory factor spinal cord injury
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C-X-C chemokine receptor type 7 antibody enhances neural plasticity after ischemic stroke 被引量:1
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作者 Xiao-Qian Zhang Xiao-Yin Wang +4 位作者 Bing-Chao Dong Mei-Xuan Li Yu Wang Ting Xiao Shan-Shan Zhao 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第9期1976-1982,共7页
Stromal cell-derived factor-1 and its receptor C-X-C chemokine receptor 4(CXCR4) have been shown to regulate neural regeneration after stroke.Howeve r,whether stromal cell-derived factor-1 receptor CXCR7,which is wide... Stromal cell-derived factor-1 and its receptor C-X-C chemokine receptor 4(CXCR4) have been shown to regulate neural regeneration after stroke.Howeve r,whether stromal cell-derived factor-1 receptor CXCR7,which is widely distributed in the develo ping and adult central nervous system,participates in neural regeneration remains poorly unde rstood.In this study,we established rat models of focal cerebral ischemia by injecting endothelin-1 into the cerebral co rtex and striatum.Starting on day 7 after injury,CXCR7-neutralizing antibody was injected into the lateral ventricle using a micro drug delivery system for 6 consecutive days.Our results showed that CXCR7-neutralizing antibody increased the total length and number of sprouting co rticospinal tra ct fibers in rats with cerebral ischemia,increased the expression of vesicular glutamate transporter 1 and growth-related protein 43,marke rs of the denervated spinal cord synapses,and promoted the differentiation and maturation of oligodendrocyte progenitor cells in the striatum.In addition,CXCR7 antibody increased the expression of CXCR4 in the striatum,increased the protein expression of RAS and ERK1/2 associated with the RAS/ERK signaling pathway,and im proved rat motor function.These findings suggest that CXCR7 improved neural functional recovery after ischemic stroke by promoting axonal regeneration,synaptogenesis,and myelin regeneration,which may be achieved by activation of CXCR4 and the RAS/ERK1/2 signaling pathway. 展开更多
关键词 axonal regeneration cerebral ischemia C-X-C chemokine receptor 4 CXCR7 antibody neural plasticity RAS/ERK pathway REMYELINATION stroke stromal cell-derived factor-1 SYNAPTOGENESIS
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C-C chemokine receptor type 2-overexpressing exosomes alleviated experimental post-stroke cognitive impairment by enhancing microglia/macrophage M2 polarization 被引量:7
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作者 Huai-Chun Yang Min Zhang +5 位作者 Rui Wu Hai-Qing Zheng Li-Ying Zhang Jing Luo Li-Li Li Xi-Quan Hu 《World Journal of Stem Cells》 SCIE 2020年第2期152-167,共16页
BACKGROUND Human-derived mesenchymal stromal cells have been shown to improve cognitive function following experimental stroke.The activity of exosomes has been verified to be comparable to the therapeutic effects of ... BACKGROUND Human-derived mesenchymal stromal cells have been shown to improve cognitive function following experimental stroke.The activity of exosomes has been verified to be comparable to the therapeutic effects of mesenchymal stromal cells.However,the effects of exosomes derived from human umbilical cord mesenchymal stem cells(HUC-MSCs)(ExoCtrl)on post-stroke cognitive impairment(PSCI)have rarely been reported.Moreover,whether exosomes derived from C-C chemokine receptor type 2(CCR2)-overexpressing HUC-MSCs(ExoCCR2)can enhance the therapeutic effects on PSCI and the possible underlying mechanisms have not been studied.AIM To investigate the effects of ExoCtrl on PSCI and whether ExoCCR2 can enhance therapeutic effects on PSCI.METHODS Transmission electron microscopy,qNano®particles analyzer,and Western blotting were employed to determine the morphology and CCR2 expression of ExoCtrl or ExoCCR2.ELISA was used to study the binding capacity of exosomes to CC chemokine ligand 2(CCL2)in vivo.After the intravenous injection of ExoCtrl or ExoCCR2 into experimental rats,the effect of ExoCtrl and ExoCCR2 on PSCI was assessed by Morris water maze.Remyelination and oligodendrogenesis were analyzed by Western blotting and immunofluorescence microscopy.QRT-PCR and immunofluorescence microscopy were conducted to compare the microglia/macrophage polarization.The infiltration and activation of hematogenous macrophages were analyzed by Western blotting and transwell migration analysis.RESULTS CCR2-overexpressing HUC-MSCs loaded the CCR2 receptor into their exosomes.The morphology and diameter distribution between ExoCtrl and ExoCCR2 showed no significant difference.ExoCCR2 bound significantly to CCL2 but ExoCtrl showed little CCL2 binding.Although both ExoCCR2 and ExoCtrl showed beneficial effects on PSCI,oligodendrogenesis,remyelination,and microglia/macrophage polarization,ExoCCR2 exhibited a significantly superior beneficial effect.We also found that ExoCCR2 could suppress the CCL2-induced macrophage migration and activation in vivo and in vitro,compared with ExoCtrl treated group.CONCLUSION CCR2 over-expression enhanced the therapeutic effects of exosomes on the experimental PSCI by promoting M2 microglia/macrophage polarization,enhancing oligodendrogenesis and remyelination.These therapeutic effects are likely through suppressing the CCL2-induced hematogenous macrophage migration and activation.Key words:Cognitive impairment;Stroke;Exosomes;C-C chemokine receptor type 2;Microglia/macrophage polarization;Remyelination. 展开更多
关键词 Cognitive impairment Stroke EXOSOMES c-c chemokine receptor type 2 Microglia/macrophage polarization REMYELINATION
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前列腺癌相关成纤维细胞通过分泌趋化因子C-C基元配体15促进单核细胞迁移
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作者 邵毅 宋圣举 +1 位作者 韩瑞发 尚芝群 《中国中西医结合外科杂志》 CAS 2024年第5期633-636,共4页
目的:探究前列腺癌微环境中趋化因子C-C基元配体15(CCL15)的表达、来源以及对单核细胞迁移能力的影响。方法:对正常前列腺组织和前列腺癌组织进行CCL15免疫荧光染色,使用免疫组化和免疫荧光双染实验探究CCL15的主要来源细胞。从新鲜的... 目的:探究前列腺癌微环境中趋化因子C-C基元配体15(CCL15)的表达、来源以及对单核细胞迁移能力的影响。方法:对正常前列腺组织和前列腺癌组织进行CCL15免疫荧光染色,使用免疫组化和免疫荧光双染实验探究CCL15的主要来源细胞。从新鲜的正常前列腺组织和前列腺癌组织中分离成纤维细胞并进行原代培养,通过实时定量PCR、免疫印迹实验和ELISA实验检测成纤维细胞中α-平滑肌肌动蛋白(α-SMA)、成纤维细胞活化蛋白(FAP)、波形蛋白(Vimentin)和CCL15的表达情况。利用慢病毒转染敲低CCL15,探究敲低CCL15后成纤维细胞条件培养基对单核细胞迁移能力的影响。进行多色免疫荧光染色检测前列腺癌组织中CCL15与M2巨噬细胞的位置关系。结果:前列腺癌组织中CCL15的表达明显高于正常组织,且主要来源于表达α-SMA的成纤维细胞。与前列腺正常成纤维细胞(NF)相比,前列腺癌相关成纤维细胞(CAF)分泌CCL15的能力显著增强。敲低CCL15后,前列腺CAF分泌的CCL15明显减少,减弱了单核细胞的迁移能力。在前列腺癌组织中,CCL15高表达区域存在更多M2巨噬细胞。结论:前列腺CAF通过分泌CCL15促进单核细胞迁移,增加前列腺癌微环境中M2巨噬细胞的浸润。 展开更多
关键词 前列腺癌 成纤维细胞 单核细胞 免疫微环境 趋化因子c-c基元配体15
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离子推力器C-C复合栅多工况热态微位移研究
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作者 高斌 李娟 +2 位作者 陈娟娟 李如月 王彦龙 《真空》 CAS 2024年第5期90-96,共7页
针对LIPS-100离子推力器C-C一体化复合栅极组件设计问题,利用热特性计算模型开展栅极热力学特性研究。采用Workbench瞬态热分析法研究了两种曲面朝向的C-C栅极热性能参数,并与传统金属钼栅进行了对比分析。结果表明:等工况、等球面构型... 针对LIPS-100离子推力器C-C一体化复合栅极组件设计问题,利用热特性计算模型开展栅极热力学特性研究。采用Workbench瞬态热分析法研究了两种曲面朝向的C-C栅极热性能参数,并与传统金属钼栅进行了对比分析。结果表明:等工况、等球面构型、等栅间距条件下,C-C复合栅较钼栅组件质量减轻35.7%,热态分析温度上限降低19.6%,升温速率降低21.3%;C-C复合屏栅较钼栅微位移减小0.151 mm,加速栅微位移减小0.123 mm,具有更高的抗热冲击性,可有效缓解推力器工作前期栅间距波动较大的问题;同一C-C复合栅材料下,球面朝向结构不同,栅极中心-开孔区边缘热态微位移不同,凸型栅较凹型栅加速栅微位移量降低0.025~0.038 mm,可有效提升加速栅开孔区磨损寿命。对于小尺寸离子推力器,凸面C-C复合栅组件抗热冲击性优势明显。 展开更多
关键词 离子推力器 栅极组件 c-c复合材料 热形变位移
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Chemokine Receptors CCR1, CCR3, CCR7 and Chemokines CX3CL1 and CCL5 are Significantly Up-Regulated and Very Reliable for Acute Rejection Diagnosis of Kidney Transplants
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作者 Paula Xavier Dias-Pinto José Gerardo G. Oliveira 《Open Journal of Nephrology》 2023年第2期126-149,共24页
Background: The allo-immune response following organ transplantation constitutes one of the main determinants concerning both short- and long- term outcomes in renal graft recipients. Chemokines and their receptors pl... Background: The allo-immune response following organ transplantation constitutes one of the main determinants concerning both short- and long- term outcomes in renal graft recipients. Chemokines and their receptors play a diversified and important role, either homeostatic or inflammatory and direct different immune-competent cell types to the allograft. While deeply studied in the last two decades, controversy persists as a result of chemokines’ pleiotropic actions. We report our analysis of CCR1, CCR3, CCR7, CCL5 and CX3CL1 expression or synthesis by graft-infiltrating cells in human kidney transplants (KTx). At the same time, we tested their robustness in diagnosing acute rejection. Methods: Fine-needle aspiration biopsies (Fnab) were performed either on days 7 or 14 post-transplantation among stable KTx and on the day of acute rejection (AR) diagnosis. Fnab cytopreparations were studied by the enzymatic avidin-biotin complex staining for CCR1, CCR3, CCR7 and CX3CL1. From another subgroup of cases, Fnab samples were cultured for 48 hours and the supernatants were analysed for CCL5 by ELISA. Results: The group of AR cases showed a significantly up-regulated expression of CCR1, CCR3, CCR7 and CX3CL1 and a significantly higher synthesis of CCL5. The positive predictive values were respectively 92%, 97%, 85%, 76% and 78% and negative predictive values were by the same order, 100%, 73%, 100%, 98% and 83%. Conclusions: Our study permits us to advance that CCR1 and CCR3 play a significant and non-redundant role in acute rejection, and it is the first report of CCR3 association with rejection, probably related to CCL5. The presence inside the graft of significant up-regulation for CCR7 surmises that part of antigen presentation may be performed there without being restricted to secondary lymphoid sites. Our results with CX3CL1 confirm other reports. 展开更多
关键词 Kidney Transplants Aspiration Biopsies Acute Rejection chemokineS chemokine Receptors
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Neuronal chemokines:new insights into neuronal communication after injury
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作者 Francina Mesquida-Veny Arnau Hervera 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第11期2379-2380,共2页
Classically,chemokines were described as small proteins driving leukocyte migration.Nonetheless,more and more studies are showing the great variety of cell functions and tissues in which they participate,including neu... Classically,chemokines were described as small proteins driving leukocyte migration.Nonetheless,more and more studies are showing the great variety of cell functions and tissues in which they participate,including neural cells.During the last years,research has highlighted the importance of chemokines in the nervous system,governing a wide range of processes (MesquidaVeny et al.,2021).This is evidenced for example by the crucial role played by CXCL12 during cortical development,or the homeostatic role of neuronal CX3CL1,preventing microglial activation.We are now certain that many chemokines and their receptors are widely expressed in neurons,and growing evidence has shown them as fundamental players in direct neuronal communication,both during homeostasis and after insult. 展开更多
关键词 CXCL12 chemokine
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乌头碱调节C-C基序趋化因子配体2/C-C基序趋化因子受体2信号通路对膀胱癌细胞抗肿瘤活性及其作用机制研究
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作者 任慧云 冯一伟 许培英 《安徽医药》 CAS 2024年第4期660-665,I0001,共7页
目的 探讨乌头碱调节C-C基序趋化因子配体2(CCL2)/C-C基序趋化因子受体2(CCR2)信号通路对膀胱癌细胞抗肿瘤活性及其作用机制研究。方法 研究起止时间为2021年12月至2022年10月。采用细胞计数试剂盒(CCK-8)法检测2.5、5.0、10.0、20.0、3... 目的 探讨乌头碱调节C-C基序趋化因子配体2(CCL2)/C-C基序趋化因子受体2(CCR2)信号通路对膀胱癌细胞抗肿瘤活性及其作用机制研究。方法 研究起止时间为2021年12月至2022年10月。采用细胞计数试剂盒(CCK-8)法检测2.5、5.0、10.0、20.0、30.0μmol/L乌头碱处理后的人膀胱癌5637细胞存活率,筛选出合适的乌头碱作用浓度。将5637细胞分为对照组、乌头碱低剂量(10μmol/L)组、乌头碱高剂量(20μmol/L)组、乌头碱高剂量(20μmol/L)+空载组、乌头碱高剂量(20μmol/L)+CCL2过表达组,分组处理后,采用CCK-8法、5-乙炔基-2’-脱氧尿苷(Edu)染色法及Hoechst 33258染色分别检测各组5637细胞存活率、增殖率、凋亡率;采用Transwell实验及划痕实验分别检测各组5637细胞侵袭数、迁移率;采用免疫荧光染色检测各组5637细胞凋亡相关蛋白BCL2相关X蛋白(Bax)和B淋巴细胞瘤-2(Bcl-2)表达比值(Bax/Bcl-2);采用免疫印迹法检测各组5637细胞CCL2/CCR2信号通路相关蛋白及上皮间质转化标志蛋白[神经钙黏素(N-cadherin)、锌指E盒结合同源盒1(ZEB1)、紧密连接蛋白1(ZO-1)、上皮钙黏素(E-cadherin)]表达。结果 与对照组相比,乌头碱低剂量组、乌头碱高剂量组、乌头碱高剂量+空载组细胞CCL2(0.69±0.09、0.20±0.03、0.19±0.04比1.21±0.13),CCR2(0.78±0.12、0.26±0.06、0.27±0.07比1.33±0.20)、Ncadherin(0.65±0.06、0.12±0.02、0.11±0.03比1.24±0.12)与ZEB1蛋白表达、存活率、增殖率、侵袭数、迁移率均降低(P<0.05),Bax/Bcl-2、细胞ZO-1与E-cadherin蛋白表达均升高(P<0.05);乌头碱高剂量组、乌头碱高剂量+空载组细胞CCL2、CCR2、N-cadherin与ZEB1蛋白表达、存活率、增殖率、侵袭数、迁移率相比乌头碱低剂量组进一步降低(P<0.05),Bax/Bcl-2、细胞ZO-1与Ecadherin蛋白表达进一步升高(P<0.05)。与乌头碱高剂量组相比,乌头碱高剂量+CCL2过表达组细胞CCL2、CCR2、N-cadherin与ZEB1蛋白表达、存活率、增殖率、侵袭数、迁移率升高(P<0.05),Bax/Bcl-2、细胞ZO-1与E-cadherin蛋白表达降低(P<0.05)。结论 乌头碱可通过CCL2/CCR2信号通路而抑制膀胱癌细胞存活、增殖及侵袭和迁移,促使其凋亡。 展开更多
关键词 乌头碱 c-c基序趋化因子配体2/c-c基序趋化因子受体2 信号通路 膀胱癌 抗肿瘤
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银离子促进神经传导素分子内氢原子转移和C-C键解离反应
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作者 易秋浩 吴海铭 骆智训 《Chinese Journal of Chemical Physics》 SCIE EI CAS CSCD 2024年第2期341-350,I0104,共11页
色氨酸、酪氨酸和组氨酸是三种基本的氨基酸,也是大脑营养代谢中重要神经传导素的前驱体。本文利用自制的反射式时间飞行质谱仪结合磁控溅射束源和下联管式反应器,在气相条件下研究了这三个氨基酸与银离子的相互作用,揭示了这些有机小... 色氨酸、酪氨酸和组氨酸是三种基本的氨基酸,也是大脑营养代谢中重要神经传导素的前驱体。本文利用自制的反射式时间飞行质谱仪结合磁控溅射束源和下联管式反应器,在气相条件下研究了这三个氨基酸与银离子的相互作用,揭示了这些有机小分子在银离子的存在下容易解离并产生碎片和产物重组的现象,并利用密度泛函理论计算,阐明了其中的反应机制。研究发现,银离子能促进氢原子转移,进而影响竞争性的C_(α)-C_(β)和C_(β)-C_(γ)键解离反应。本研究丰富了对这类神经传导素分子基本规律与性质的精准认识,从而有助于深入理解生物体内类似生理过程的化学机制。 展开更多
关键词 神经传导素 色氨酸 金属-有机相互作用 c-c键解离 质谱
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蓝光诱导苯基重氮乙酸酯与1,3-二酮的C-C键插入反应
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作者 艾星彤 胡丽萍 +1 位作者 周从山 李立军 《化学研究》 CAS 2024年第1期23-28,共6页
卡宾是有机合成中的一类重要的活性中间体,可发生丰富的化学转化,在C-C键、C-H键、C-N键、C-O键和C-S键等构建中有重要应用。采用重氮化合物为卡宾前驱原料,在蓝光诱导下与1,3-二羰基化合物进行反应,合成了全碳季碳中心的1,4-二羰基产... 卡宾是有机合成中的一类重要的活性中间体,可发生丰富的化学转化,在C-C键、C-H键、C-N键、C-O键和C-S键等构建中有重要应用。采用重氮化合物为卡宾前驱原料,在蓝光诱导下与1,3-二羰基化合物进行反应,合成了全碳季碳中心的1,4-二羰基产物。该方法的特点是不使用金属催化剂、有良好的产率和选择性、操作简单、绿色环保无污染。 展开更多
关键词 蓝光 重氮化合物 1 3-二酮 c-c键插入反应
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A review on electrocatalytic CO_(2) conversion via C-C and C-N coupling
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作者 Zhuangzhi Zhang Sijun Li +6 位作者 Zheng Zhang Zhou Chen Hua Wang Xianguang Meng Wenquan Cui Xiwei Qi Jiacheng Wang 《Carbon Energy》 SCIE EI CAS CSCD 2024年第2期167-194,共28页
Electrochemical C-C and C-N coupling reactions with the conversion of abundant and inexpensive small molecules,such as CO_(2) and nitrogencontaining species,are considered a promising route for increasing the value of... Electrochemical C-C and C-N coupling reactions with the conversion of abundant and inexpensive small molecules,such as CO_(2) and nitrogencontaining species,are considered a promising route for increasing the value of CO_(2) reduction products.The development of high-performance catalysts is the key to the both electrocatalytic reactions.In this review,we present a systematic summary of the reaction systems for electrocatalytic CO_(2) reduction,along with the coupling mechanisms of C-C and C-N bonds over outstanding electrocatalytic materials recently developed.The key intermediate species and reaction pathways related to the coupling as well as the catalyst-structure relationship will be also discussed,aiming to provide insights and guidance for designing efficient CO_(2) reduction systems. 展开更多
关键词 c-c coupling C-N coupling CO_(2) conversion ELECTROCATALYSIS urea synthesis
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Blocking postsynaptic density-93 binding to C-X3-C motif chemokine ligand 1 promotes microglial phenotypic transformation during acute ischemic stroke
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作者 Xiao-Wei Cao Hui Yang +6 位作者 Xiao-Mei Liu Shi-Ying Lou Li-Ping Kong Liang-Qun Rong Jun-Jun Shan Yun Xu Qing-Xiu Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第5期1033-1039,共7页
We previously reported that postsynaptic density-93 mediates neuron-microglia crosstalk by interacting with amino acids 357–395 of C-X3-C motif chemokine ligand 1(CX3 CL1) to induce microglia polarization. More impor... We previously reported that postsynaptic density-93 mediates neuron-microglia crosstalk by interacting with amino acids 357–395 of C-X3-C motif chemokine ligand 1(CX3 CL1) to induce microglia polarization. More importantly, the peptide Tat-CX3 CL1(comprising amino acids 357–395 of CX3 CL1) disrupts the interaction between postsynaptic density-93 and CX3 CL1, reducing neurological impairment and exerting a protective effect in the context of acute ischemic stroke. However, the mechanism underlying these effects remains unclear. In the current study, we found that the pro-inflammatory M1 phenotype increased and the anti-inflammatory M2 phenotype decreased at different time points. The M1 phenotype increased at 6 hours after stroke and peaked at 24 hours after perfusion, whereas the M2 phenotype decreased at 6 and 24 hours following reperfusion. We found that the peptide Tat-CX3 CL1(357–395 aa) facilitates microglial polarization from M1 to M2 by reducing the production of soluble CX3 CL1. Furthermore, the a disintegrin and metalloprotease domain 17(ADAM17) inhibitor GW280264 x, which inhibits metalloprotease activity and prevents CX3 CL1 from being sheared into its soluble form, facilitated microglial polarization from M1 to M2 by inhibiting soluble CX3 CL1 formation. Additionally, Tat-CX3 CL1(357–395 aa) attenuated long-term cognitive deficits and improved white matter integrity as determined by the Morris water maze test at 31–34 days following surgery and immunofluorescence staining at 35 days after stroke, respectively. In conclusion, Tat-CX3 CL1(357–395 aa) facilitates functional recovery after ischemic stroke by promoting microglial polarization from M1 to M2. Therefore, the Tat-CX3 CL1(357–395 aa) is a potential therapeutic agent for ischemic stroke. 展开更多
关键词 a disintegrin and metalloprotease domain 17 cerebral ischemia/reperfusion C-X3-C motif chemokine ligand 1 GW280264x microglia neuroinflammation postsynaptic density-93 Tat-CX3CL1(357–395aa)
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CC-chemokine receptor 7 and its ligand CCL 19 promote mitral valve interstitial cell migration and repair
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作者 Xiaozhi Wang Liang Wang +3 位作者 Liping Miao Rong Zhao Yanhu Wu Xiangqing Kong 《The Journal of Biomedical Research》 CAS CSCD 2015年第6期456-464,共9页
The effect of CC-chemokine receptor 7 (CCR7) and CC-chemokine ligand 19 (CCL19) on rheumatic mitral ste- nosis is unknown. This study aimed to explore the roles of CCR7 and CCL19 in rheumatic mitral stenosis by me... The effect of CC-chemokine receptor 7 (CCR7) and CC-chemokine ligand 19 (CCL19) on rheumatic mitral ste- nosis is unknown. This study aimed to explore the roles of CCR7 and CCL19 in rheumatic mitral stenosis by mea- suring the expression of CCR7 and CCL19 in human mitral valves from rheumatic mitral stenosis patients. Additionally, we examined their effects on human mitral valve interstitial cells (hMVICs) proliferation, apoptosis and wound repair. CCR7 and CCL19 expression was measured in the mitral valves from rheumatic mitral stenosis patients (n= 10) and compared to normal mitral valves (n=5). CCR7 was measured in cultured hMVICs from rheu- matic mitral stenosis patients and normal donors by RT-PCR and immunofluorescence. The cells were also treated with exogenous CCL19, and the effects on wound healing, proliferation and apoptosis were assayed. In the rheu- matic mitral valves, valve interstitial cells expressed CCR7, while mononuclear cells and the endothelium expressed CCL19. Healthy mitral valves did not stain positive for CCR7 or CCL19. CCR7 was also detected in cultured rheu- matic hMVICs or in normal hMVICs treated with CCL19. In a wound healing experiment, wound closure rates of both rheumatic and normal hMVICs were significantly accelerated by CCL19. These effects were abrogated by a CCR7 neutralizing antibody. The CCR7/CCL19 axis did not influence the proliferation or apoptosis of hMVICs, indicating that wound healing was due to increased migration rates rather than increased proliferation. In conclu- sion, CCR7 and CCL19 were expressed in rheumatic mitral valves. The CCR7/CCL19 axis may regulate remodel- ing of rheumatic valve injury through promoting migratory ability of hMVICs. 展开更多
关键词 CC-chemokine receptor 7 CC-chemokine ligand 19 rheumatic mitral stenosis migration woundrepair
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血清白三烯C4、D4及C-C趋化因子配体21水平与腺样体肥大患儿腺样体肥大程度及预后的相关性 被引量:2
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作者 刘晓峰 杜娟 +4 位作者 王登茂 王亚芳 崔莉 宋英鸾 耿江桥 《川北医学院学报》 CAS 2023年第7期927-930,共4页
目的:探讨血清白三烯C4(LTC4)、D4(LTC4)及C-C趋化因子配体21(CCL21)水平与腺样体肥大患儿腺样体肥大程度及预后的相关性。方法:选取82例腺样体肥大患儿为研究对象,根据腺体样肥大程度将患儿分为中度组(n=48)和重度组(n=34),根据不同预... 目的:探讨血清白三烯C4(LTC4)、D4(LTC4)及C-C趋化因子配体21(CCL21)水平与腺样体肥大患儿腺样体肥大程度及预后的相关性。方法:选取82例腺样体肥大患儿为研究对象,根据腺体样肥大程度将患儿分为中度组(n=48)和重度组(n=34),根据不同预后分为非增生组(预后良好,n=65)和再增生组(预后不良,n=17)。比较各组患儿血清LTC4、LTC4、CCL21水平;采用受试者特征工作曲线(ROC曲线)评估上述指标对腺样体肥大患儿预后不良的预测价值。结果:重度组患儿血清LTC4、LTD4、CCL21水平高于中度组(P<0.05);再增生组患儿血清LTC4、LTD4、CCL21水平均高于非增生组(P<0.05)。ROC曲线分析显示,当LTC4≥346.68 ng/L时,预测腺样体肥大患儿预后不良的曲线下面积(AUC)为0.789,敏感度为0.706,特异度为0.738;当LTD4≥270.19 ng/L时,预测腺样体肥大患儿预后不良的AUC为0.665,敏感度为0.765,特异度为0.600;当CCL21≥144.57 ng/mL时,预测腺样体肥大患儿预后不良的AUC为0.738,敏感度为0.706,特异度为0.692;三者联合预测的AUC为0.853,敏感度为0.882,特异度为0.769。结论:血清LTC4、LTD4及CCL21水平与腺样体肥大患儿腺样体肥大程度及预后密切相关,可将三者联合检测用于腺样体肥大患儿预后不良的辅助预测。 展开更多
关键词 白三烯C4 白三烯D4 c-c趋化因子配体21 腺样体肥大 预后
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CXC chemokines and chemokine receptors in gastric cancer: From basic findings towards therapeutic targeting 被引量:25
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作者 Hyo Jin Lee Ik-Chan Song +2 位作者 Hwan-Jung Yun Deog-Yeon Jo Samyong Kim 《World Journal of Gastroenterology》 SCIE CAS 2014年第7期1681-1693,共13页
Gastric cancer is the fourth most common cancer,and the second-highest cause of cancer-related deaths worldwide.Despite extensive research to identify novel diagnostic and therapeutic agents,patients with advanced gas... Gastric cancer is the fourth most common cancer,and the second-highest cause of cancer-related deaths worldwide.Despite extensive research to identify novel diagnostic and therapeutic agents,patients with advanced gastric cancer suffer from a poor quality of life and poor prognosis,and treatment is dependent mainly on conventional cytotoxic chemotherapy.To improve the quality of life and survival of gastric cancer patients,a better understanding of the underlying molecular pathologies,and their application towards the development of novel targeted therapies,is urgently needed.Chemokines are a group of small proteins associated with cytoskeletal rearrangements,the directional migration of several cell types during development and physiology,and the host immune response via interactions with G-protein coupled receptors.There is also growing evidence to suggest that chemokines not only play a role in the immune system,but are also involved in the development and progression of tumors.In gastric cancer,CXC chemokines and chemokine receptors regulate the trafficking of cells in and out of the tumor microenvironment.CXC chemokines and their receptors can also directly influence tumorigenesis by modulating tumor transformation,survival,growth,invasion and metastasis,as well as indirectly by regulating angiogenesis,and tumor-leukocyte interactions.In this review,we will focus on the roles of CXC chemokines and their receptors in the development,progression,and metastasis of gastric tumors,and discuss their therapeutic potential for gastric cancer. 展开更多
关键词 chemokine chemokine receptor Gastric neoplasm Therapeutic target
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Chemokines play complex roles in cerebral ischemia 被引量:10
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作者 CHEN Chen CHU Shi-feng +4 位作者 LIU Dan-dan ZHANG Zhao KONG Ling-lei ZHOU Xin CHEN Nai-hong 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2018年第9期672-673,共2页
Ischemic stroke(IS) is a disease caused by deficiency of blood and oxygen in focal or complete brain,followed by inflammation cascade and other pathological reactions,which finally lead to irreversible damage to the c... Ischemic stroke(IS) is a disease caused by deficiency of blood and oxygen in focal or complete brain,followed by inflammation cascade and other pathological reactions,which finally lead to irreversible damage to the cerebrum.For the inflammation is a key progress at the initiation of ischemia and poststroke,and chemokines work as vital cytokines in inflammation,we focus the roles of chemokines in IS.Studies have shown cerebral ischemia is associated with marked induction of both CXC and CC chemokines which resulting in extensive leukocyte infiltration in the ischemic brain,and neutrophil infiltration may increase cerebral edema inducing injury in the ischemic area.In addition,chemokines also shows other functions such as promote neuroblast migration,hematogenous cell recruitment and functional brain repair.Thus,a similar chemokine ligand/chemokine receptor pair can mediate both beneficial and detrimental effects depending on the window of observation and pathophysiological conditions.This manuscript reviews the studies about chemokine-mediated effects in cerebral ischemia/reperfusion and discusses the potential significance of these interactions in injury and repair of ischemic tissues.We also refer drug development based on the chemokines and clinical applications using chemokines as diagnostic or prognostic biomarkers in ischemic stroke. 展开更多
关键词 chemokine CEREBRAL ISCHEMIA ISCHEMIC stroke
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