Login Register Cart 0
Generic placeholder image

当代阿耳茨海默病研究

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe Translate in English
Review Article

小胶质细胞存储钙离子在健康和阿尔茨海默氏病中的作用

卷 17, 期 12, 2020

页: [1057 - 1064] 页: 8

弟呕挨: 10.2174/1567205018666210119143817

价格: $65

摘要

神经元中钙信号传导机制的失调被认为是早发性阿尔茨海默氏病（AD）发病机理的一个促成因素。然而，关于驻留免疫细胞小胶质细胞中Ca2 +动员可能受到损害的了解知之甚少。这项审查考虑的发现表明，非兴奋性小胶质细胞的一个显着途径，即储库操作的钙进入（SOCE），在散发性的AD中被改变了。首先讨论了通过血小板活化因子（PAF）刺激健康大脑中成年，胎儿和永生化细胞系，人小胶质细胞中SOCE的Ca2 +动员模式。在所有情况下，都发现PAF会引起内质网（ER）存储中Ca2 +的快速瞬时消耗，然后持续进入Ca2 +（SOCE）。 ATP刺激人小胶质细胞观察到SOCE的持续时间大大缩短，这是由于对不同亚型嘌呤能受体的激动作用所致。从AD脑组织获得的小胶质细胞，或用全长淀粉样β-肽（Aβ42）处理的小胶质细胞，相对于对照，SOCE振幅显着降低。此外，与对照组相比，AD脑和经Aβ42处理的小胶质细胞从ER储存释放的Ca2 +释放水平降低。小胶质细胞中SOCE的性质变化可能导致发炎的AD脑中免疫细胞反应改变和神经血管单位功能障碍。

关键词: 人类小胶质细胞，钙储运钙（SOCE），血小板活化因子（PAF），长期SOCE，β-淀粉样蛋白（Aβ），阿尔茨海默氏病（AD）。

« Previous Next »
[1]
Wake H, Moorhouse AJ, Jinno S, Kohsaka S, Nabekura J. Resting microglia directly monitor the functional state of synapses in vivo and determine the fate of ischemic terminals. J Neurosci 2009; 29(13): 3974-80.
[http://dx.doi.org/10.1523/JNEUROSCI.4363-08.2009] [PMID: 19339593]
[2]
Combs CK, Johnson DE, Cannady SB, Lehman TM, Landreth GE. Identification of microglial signal transduction pathways mediating a neurotoxic response to amyloidogenic fragments of β-amyloid and prion proteins. J Neurosci 1999; 19(3): 928-39.
[http://dx.doi.org/10.1523/JNEUROSCI.19-03-00928.1999] [PMID: 9920656]
[3]
McDonald DR, Brunden KR, Landreth GE. Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia. J Neurosci 1997; 17(7): 2284-94.
[http://dx.doi.org/10.1523/JNEUROSCI.17-07-02284.1997] [PMID: 9065490]
[4]
Bamberger ME, Harris ME, McDonald DR, Husemann J, Landreth GE. A cell surface receptor complex for fibrillar β-amyloid mediates microglial activation. J Neurosci 2003; 23(7): 2665-74.
[http://dx.doi.org/10.1523/JNEUROSCI.23-07-02665.2003] [PMID: 12684452]
[5]
McLarnon JG, Xu R, Lee YB, Kim SU. Ion channels of human microglia in culture. Neuroscience 1997; 78(4): 1217-28.
[http://dx.doi.org/10.1016/S0306-4522(96)00680-X] [PMID: 9174088]
[6]
Eder C. Ion channels in microglia (brain macrophages). Am J Physiol 1998; 275(2): C327-42.
[http://dx.doi.org/10.1152/ajpcell.1998.275.2.C327] [PMID: 9688586]
[7]
Secondo A, Bagetta G, Amantea D. On the role of store-operated calcium entry in acute and chronic neurodegenerative diseases. Front Mol Neurosci 2018; 11: 87.
[http://dx.doi.org/10.3389/fnmol.2018.00087] [PMID: 29623030]
[8]
Hemonnat AL, Hua J, Ulmann L, Hirbec H. Microglia in Alzheimer’s disease: Well-known targets and new opportunities Front Aging Neurosci 2019; 11: 233.
[http://dx.doi.org/10.3389/fnagi.2019.00233]
[9]
Lewis RS. Store-operated calcium channels: New perspectives on mechanism and function. Cold Spring Harb Perspect Biol 2011; 3(12)a003970
[10]
Putney JW, Steinckwich-Besançon N, Numaga-Tomita T, et al. The functions of store-operated calcium channels. Biochim Biophys Acta Mol Cell Res 2017; 1864(6): 900-6.
[http://dx.doi.org/10.1016/j.bbamcr.2016.11.028] [PMID: 27913208]
[11]
Putney JW. Forms and functions of store-operated calcium entry mediators, STIM and Orai. Adv Biol Regul 2018; 68: 88-96.
[http://dx.doi.org/10.1016/j.jbior.2017.11.006] [PMID: 29217255]
[12]
Lewis RS. Store-operated calcium channels: From function to structure and back again. Cold Spring Harb Perspect Biol 2020; 12(5)a035055
[http://dx.doi.org/10.1101/cshperspect.a035055] [PMID: 31570335]
[13]
Prakriya M, Lewis RS. Store-operated calcium channels. Physiol Rev 2015; 95(4): 1383-436.
[http://dx.doi.org/10.1152/physrev.00020.2014] [PMID: 26400989]
[14]
Hogan PG, Rao A. Store-operated calcium entry: Mechanisms and modulation. Biochem Biophys Res Commun 2015; 460(1): 40-9.
[http://dx.doi.org/10.1016/j.bbrc.2015.02.110] [PMID: 25998732]
[15]
Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 2002; 297(5580): 353-6.
[http://dx.doi.org/10.1126/science.1072994] [PMID: 12130773]
[16]
Wang H, Liu S, Tian Y, et al. Quetiapine inhibits microglial activation by neutralizing abnormal STIM1-mediated intercellular calcium homeostasis and promotes myelin repair in a cuprizone-induced mouse model of demyelination. Front Cell Neurosci 2015; 9: 492.
[http://dx.doi.org/10.3389/fncel.2015.00492] [PMID: 26732345]
[17]
Michaelis M, Nieswandt B, Stegner D, Eilers J, Kraft R. STIM1, STIM2, and Orai1 regulate store-operated calcium entry and purinergic activation of microglia. Glia 2015; 63(4): 652-63.
[http://dx.doi.org/10.1002/glia.22775] [PMID: 25471906]
[18]
Gilbert DF, Stebbing MJ, Kuenzel K, et al. Store-operated Ca2+ entry (SOCE) and purinergic receptor-mediated Ca2+ homeostasis in murine bv2 microglial cells: Early cellular responses to ATP-mediated microglia activation. Front Mol Neurosci 2016; 9: 111.
[19]
Heo DK, Lim HM, Nam JH, Lee MG, Kim JY. Regulation of phagocytosis and cytokine secretion by store-operated calcium entry in primary isolated murine microglia. Cell Signal 2015; 27(1): 177-86.
[http://dx.doi.org/10.1016/j.cellsig.2014.11.003] [PMID: 25451082]
[20]
Toescu EC, Möller T, Kettenmann H, Verkhratsky A. Long-term activation of capacitative Ca2+ entry in mouse microglial cells. Neuroscience 1998; 86(3): 925-35.
[http://dx.doi.org/10.1016/S0306-4522(98)00123-7] [PMID: 9692728]
[21]
Mattson MP, Chan SL. Neuronal and glial calcium signaling in Alzheimer’s disease. Cell Calcium 2003; 34(4-5): 385-97.
[http://dx.doi.org/10.1016/S0143-4160(03)00128-3] [PMID: 12909083]
[22]
Bojarski L, Herms J, Kuznicki J. Calcium dysregulation in Alzheimer’s disease. Neurochem Int 2008; 52(4-5): 621-33.
[http://dx.doi.org/10.1016/j.neuint.2007.10.002] [PMID: 18035450]
[23]
Yu JT, Chang RC, Tan L. Calcium dysregulation in Alzheimer’s disease: From mechanisms to therapeutic opportunities. Prog Neurobiol 2009; 89(3): 240-55.
[http://dx.doi.org/10.1016/j.pneurobio.2009.07.009] [PMID: 19664678]
[24]
Pchitskaya E, Popugaeva E, Bezprozvanny I. Calcium signaling and molecular mechanisms underlying neurodegenerative diseases. Cell Calcium 2018; 70: 87-94.
[http://dx.doi.org/10.1016/j.ceca.2017.06.008] [PMID: 28728834]
[25]
McLarnon JG, Helm J, Goghari V, et al. Anion channels modulate store-operated calcium influx in human microglia. Cell Calcium 2000; 28(4): 261-8.
[http://dx.doi.org/10.1054/ceca.2000.0150] [PMID: 11032781]
[26]
Mori M, Aihara M, Kume K, Hamanoue M, Kohsaka S, Shimizu T. Predominant expression of platelet-activating factor receptor in the rat brain microglia. J Neurosci 1996; 16(11): 3590-600.
[http://dx.doi.org/10.1523/JNEUROSCI.16-11-03590.1996] [PMID: 8642404]
[27]
Wang X, Bae JH, Kim SU, McLarnon JG. Platelet-activating factor induced Ca(2+) signaling in human microglia. Brain Res 1999; 842(1): 159-65.
[http://dx.doi.org/10.1016/S0006-8993(99)01849-1] [PMID: 10526106]
[28]
Sattayaprasert P, Choi HB, Chongthammakun S, McLarnon JG. Platelet-activating factor enhancement of calcium influx and interleukin-6 expression, but not production, in human microglia. J Neuroinflamm 2005; 2(1): 11.
[29]
Hong SH, Choi HB, Kim SU, McLarnon JG. Mitochondrial ligand inhibits store-operated calcium influx and COX-2 production in human microglia. J Neurosci Res 2006; 83(7): 1293-8.
[http://dx.doi.org/10.1002/jnr.20829] [PMID: 16547968]
[30]
Wang X, Kim SU, van Breemen C, McLarnon JG. Activation of purinergic P2X receptors inhibits P2Y-mediated Ca2+ influx in human microglia. Cell Calcium 2000; 27(4): 205-12.
[http://dx.doi.org/10.1054/ceca.2000.0110] [PMID: 10858666]
[31]
Park JH, Kim JN, Jang BC, Im SS, Song DK, Bae JH. Glucosamine suppresses platelet-activating factor-induced activation of microglia through inhibition of store-operated calcium influx. Environ Toxicol Pharmacol 2016; 42: 1-8.
[http://dx.doi.org/10.1016/j.etap.2015.12.014] [PMID: 26745504]
[32]
Yi HA, Yi SD, Jang BC, et al. Inhibitory effects of glucosamine on lipopolysaccharide-induced activation in microglial cells. Clin Exp Pharmacol Physiol 2005; 32(12): 1097-103.
[http://dx.doi.org/10.1111/j.1440-1681.2005.04305.x] [PMID: 16445576]
[33]
Stansley B, Post J, Hensley K. A comparative review of cell culture systems for the study of microglial biology in Alzheimer’s disease. J Neuroinflamm 2012; 9: 115.www.jneuroinflamm.com/contents/9/1/1152012
[34]
McLarnon JG, Choi HB, Lue LF, Walker DG, Kim SU. Perturbations in calcium-mediated signal transduction in microglia from Alzheimer’s disease patients. J Neurosci Res 2005; 81(3): 426-35.
[http://dx.doi.org/10.1002/jnr.20487] [PMID: 15948178]
[35]
Ronco V, Grolla AA, Glasnov TN, et al. Differential deregulation of astrocytic calcium signalling by amyloid-β, TNFα, IL-1β and LPS. Cell Calcium 2014; 55(4): 219-29.
[http://dx.doi.org/10.1016/j.ceca.2014.02.016] [PMID: 24656753]
[36]
Greotti E, Capitanio P, Wong A, Pozzan T, Pizzo P, Pendin D. Familial Alzheimer’s disease-linked presenilin mutants and intracellular Ca2+ handling: A single-organelle, FRET-based analysis. Cell Calcium 2019; 79: 44-56.
[http://dx.doi.org/10.1016/j.ceca.2019.02.005] [PMID: 30822648]
[37]
Selkoe DJ, Hardy J. The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Mol Med 2016; 8(6): 595-608.
[http://dx.doi.org/10.15252/emmm.201606210] [PMID: 27025652]
[38]
Jairaman A, Prakriya M. Molecular pharmacology of store-operated CRAC channels. Channels (Austin) 2013; 7(5): 402-14.
[http://dx.doi.org/10.4161/chan.25292] [PMID: 23807116]
[39]
McLarnon JG. Purinergic mediated changes in Ca2+ mobilization and functional responses in microglia: effects of low levels of ATP. J Neurosci Res 2005; 81(3): 349-56.

Rights & Permissions Print Cite
Article Metrics
34
2
© 2025 Bentham Science Publishers | Privacy Policy