[1]吴 滢.SDF-1/CXCR4/CXCR7信号轴在缺血性脑卒中中的作用[J].医学信息,2020,33(11):34-37.[doi:10.3969/j.issn.1006-1959.2020.11.012]
 WU Ying.The Role of SDF-1/CXCR4/CXCR7 Signal Axis in Ischemic Stroke[J].Medical Information,2020,33(11):34-37.[doi:10.3969/j.issn.1006-1959.2020.11.012]
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SDF-1/CXCR4/CXCR7信号轴在缺血性脑卒中中的作用()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
33卷
期数:
2020年11期
页码:
34-37
栏目:
综述
出版日期:
2020-06-01

文章信息/Info

Title:
The Role of SDF-1/CXCR4/CXCR7 Signal Axis in Ischemic Stroke
文章编号:
1006-1959(2020)11-0034-04
作者:
吴 滢
(上海中医药大学附属上海市中西医结合医院神经内科,上海 200082)
Author(s):
WU Ying
(Department of Neurology,Shanghai Integrated Traditional Chinese and Western Medicine Hospital,Shanghai University of Traditional Chinese Medicine,Shanghai 200082,China)
关键词:
基质细胞衍生因子-1缺血性卒中CXCR4CXCR7
Keywords:
Stromal cell-derived factor-1Ischemic strokeCXCR4CXCR7
分类号:
R743.3
DOI:
10.3969/j.issn.1006-1959.2020.11.012
文献标志码:
A
摘要:
基质细胞衍生因子-1(SDF-1)是由骨髓基质细胞产生的CXC类趋化蛋白。CXCR4和CXCR7是已知的两个由SDF-1激活的两个G蛋白偶联受体,在发育和成熟的中枢神经系统中均表达,并参与中枢神经系统中多种病理生理过程,包括脑发育、血管生成、神经变性和神经发生。脑缺血性损伤后,缺血半暗带内SDF-1水平显着增加并诱导神经功能修复,SDF-1/CXCR4/CXCR7信号传导通路可能为卒中的治疗提供新的靶点。本文主要就SDF-1/CXCR4/CXCR7的结构、在中枢神经系统中的表达、相互作用以及其在脑缺血中的作用进行综述,旨在为缺血性脑卒中的治疗提供理论参考。
Abstract:
Stromal cell-derived factor-1 (SDF-1) is a CXC-like chemotactic protein produced by bone marrow stromal cells. CXCR4 and CXCR7 are two known G protein-coupled receptors activated by SDF-1, which are both expressed in the developing and mature central nervous system and participate in various pathophysiological processes in the central nervous system, including the brain Development, angiogenesis, neurodegeneration and neurogenesis. After cerebral ischemic injury, the level of SDF-1 in the ischemic penumbra significantly increased and induced neurological function repair. The SDF-1 / CXCR4 / CXCR7 signaling pathway may provide a new target for the treatment of stroke. This article mainly reviews the structure of SDF-1 / CXCR4 / CXCR7, its expression and interaction in the central nervous system, and its role in cerebral ischemia, aiming to provide a theoretical reference for the treatment of ischemic stroke.

参考文献/References:

[1]Thomas MN,Kalnins A,Andrassy M,et al.SDF-1/CXCR4/CXCR7 is pivotal for vascular smooth muscle cell proliferation and chronic allograft vasculopathy[J].Transpl Int,2015,28(12):1426-1435.[2]Zhang Y,Zhang H,Lin S,et al.SDF-1/CXCR7 Chemokine Signaling is Induced in the Peri-Infarct Regions in Patients with Ischemic Stroke[J].Aging Dis,2018,9(2):287-295.[3]Cheng X,Wang H,Zhang X,et al.The Role of SDF-1/CXCR4/CXCR7 in Neuronal Regeneration after Cerebral Ischemia[J].Front Neurosci,2017(11):590.[4]Pozzobon T,Goldoni G,Viola A,et al.CXCR4 signaling in health and disease[J].Immunol Lett,2016(177):6-15.[5]Nagasawa T.CXCL12/SDF-1 and CXCR4[J].Front Immunol,2015(6):301.[6]Nazari A,Khorramdelazad H,Hassanshahi G.Biological/pathological functions of the CXCL12/CXCR4/CXCR7 axes in the pathogenesis of bladder cancer[J].Int J Clin Oncol,2017,22(6):991-1000.[7]Banisadr G,Podojil JR,Miller SD,et al.Pattern of CXCR7 Gene Expression in Mouse Brain Under Normal and Inflammatory Conditions[J].J Neuroimmune Pharmacol,2016,11(1):26-35.[8]Qiao N,Wang L,Wang T,et al.Inflammatory CXCL12-CXCR4/CXCR7 axis mediates G-protein signaling pathway to influence the invasion and migration of nasopharyngeal carcinoma cells[J].Tumour Biol,2016,37(6):8169-8179. [9]Ding Q,Sun J,Xie W,et al.Stemona alkaloids suppress the positive feedback loop between M2 polarization and fibroblast differentiation by inhibiting JAK2/STAT3 pathway in fibroblasts and CXCR4/PI3K/AKT1 pathway in macrophages[J].Int Immunopharmacol,2019(72):385-394.[10]Hitchinson B,Eby JM,Gao X,et al.Biased antagonism of CXCR4 avoids antagonist tolerance[J].Sci Signal,2018,11(552):eaat2214.[11]Wu KJ,Yu SJ,Shia KS,et al.A Novel CXCR4 Antagonist CX549 Induces Neuroprotection in Stroke Brain[J].Cell Transplant,2017,26(4):571-583.[12]Xu D,Li R,Wu J,et al.Drug Design Targeting the CXCR4/CXCR7/CXCL12 Pathway[J].Curr Top Med Chem,2016,16(13):1441-1451.[13]Puchert M,Engele J.The peculiarities of the SDF-1/CXCL12 system:in some cells,CXCR4 and CXCR7 sing solos,in others,they sing duets[J].Cell Tissue Res,2014,355(2):239-253.[14]Feng YF,Guo H,Yuan F,et al.Lipopolysaccharide Promotes Choroidal Neovascularization by Up-Regulation of CXCR4 and CXCR7 Expression in Choroid Endothelial Cell[J].PLoS One,2015,10(8):e0136175.[15]Zhu Y,Murakami F.Chemokine CXCL12 and its receptors in the developing central nervous system:emerging themes and future perspectives[J].Dev Neurobiol,2012,72(10):1349-1362.[16]Sánchez-Alcaniz JA,Haege S,Mueller W,et al.Cxcr7 controls neuronal migration by regulating chemokine responsiveness[J].Neuron,2011,69(1):77-90.[17]Uto-Konomi A,McKibben B,Wirtz J,et al.CXCR7 agonists inhibit the function of CXCL12 by down-regulation of CXCR4[J].Biochem Biophys Res Commun,2013,431(4):772-776.[18]Ullah TR.The role of CXCR4 in multiple myeloma:Cells’ journey from bone marrow to beyond[J].J Bone Oncol,2019(17):100253.[19]Levoye A,Balabanian K,Baleux F,et al.CXCR7 heterodimerizes with CXCR4 and regulates CXCL12-mediated G protein signaling[J].Blood,2009,113(24):6085-6093.[20]Décaillot FM,Kazmi MA,Lin Y,et al.CXCR7/CXCR4 heterodimer constitutively recruits beta-arrestin to enhance cell migration[J].J Biol Chem,2011,286(37):32188-32197.[21]Borlongan CV,Glover LE,Tajiri N,et al.The great migration of bone marrow-derived stem cells toward the ischemic brain:therapeutic implications for stroke and other neurological disorders[J].Prog Neurobiol,2011,95(2):213-228. [22]Harten SK,Ashcroft M,Maxwell PH.Prolyl hydroxylase domain inhibitors:a route to HIF activation and neuroprotection[J].Antioxid Redox Signal,2010,12(4):459-480.[23]Chang YC,Shyu WC,Lin SZ,et al.Regenerative therapy for stroke[J].Cell Transplant,2007,16(2):171-181.[24]Williams JL,Holman DW,Klein RS.Chemokines in the balance: maintenance of homeostasis and protection at CNS barriers[J].Front Cell Neurosci,2014(8):154. [25]Chen Q,Zhang M,Li Y,et al.CXCR7 Mediates Neural Progenitor Cells Migration to CXCL12 Independent of CXCR4[J].Stem Cells,2015,33(8):2574-2585. [26]Merino JJ,Bellver-Landete V,Oset-Gasque MJ,et al.CXCR4/CXCR7 molecular involvement in neuronal and neural progenitor migration: focus in CNS repair[J].J Cell Physiol,2015,230(1):27-42. [27]Liu L,Chen JX,Zhang XW,et al.Chemokine receptor 7 overexpression promotes mesenchymal stem cell migration and proliferation via secreting Chemokine ligand 12[J].Sci Rep,2018,8(1):204. [28]Bogoslovsky T,Spatz M,Chaudhry A,et al.Stromal-derived factor-1[alpha]correlates with circulating endothelial progenitor cells and with acute lesion volume in stroke patients[J].Stroke,2011,42(3):618-625.[29]Keshavarz S,Nassiri SM,Siavashi V,et al.Regulation of plasticity and biological features of endothelial progenitor cells by MSC-derived SDF-1[J].Biochim Biophys Acta Mol Cell Res,2019,1866(2):296-304.[30]Song C,Xu W,Zhang X,et al.CXCR4 antagonist AMD3100 suppresses the long-term abnormal structural changes of newborn neurons in the intraventricular kainic acid model of epilepsy[J].Mol Neurol Biol,2015(53):1518-1532.[31]Zhang XQ,Mu JW,Wang HB,et al.Increased protein expression levels of pCREB, BDNF and SDF-1/CXCR4 in the hippocampus may be associated with enhanced neurogenesis induced by environmental enrichment[J].Mol Med Rep,2016(14):2231-2237.[32]Sun X,Zhou Z,Liu T,et al.Fluoxetine enhances neurogenesis in aged rats with cortical infarcts,but this is not reflected in a behavioral recovery[J].J Mol Neurosci,2016(58):233-242. [33]Sun Y,Cheng X,Wang H,et al.dl-3-n-butylphthalide promotes neuroplasticity and motor recovery in stroke rats[J].Behav Brain Res,2017(329):67-74.[34]Xu W,Mu X,Wang H,et al.Chloride co-transporter NKCC1 inhibitor bumetanide enhances neurogenesis and behavioral recovery in rats after experimental stroke[J].Mol Neurobiol,2017(54):2406-2414.[35]Dong BC,Li MX,Wang XY,et al.Effects of CXCR7-neutralizing antibody on neurogenesis in the hippocampal dentate gyrus and cognitive function in the chronic phase of cerebral ischemia[J].Neural Regen Res,2020,15(6):1079-1085. [36]Wang Y,Xu P,Qiu L,et al.CXCR7 participates in CXCL12-mediated cell cycle and proliferation regulation in mouse neural progenitor cells[J].Curr Mol Med,2016(16):738-746.

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更新日期/Last Update: 1900-01-01