Research progress of the role of microglia in the brain injury after subarachnoid hemorrhage

PENG Shu-chen YANG Xiao-mei*

doi:10.16098/j.issn.0529-1356.2018.04,024

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Acta Anatomica Sinica ›› 2018, Vol. 49 ›› Issue (4) : 556-560. DOI: 10.16098/j.issn.0529-1356.2018.04,024

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Research progress of the role of microglia in the brain injury after subarachnoid hemorrhage

PENG Shu-chen YANG Xiao-mei*

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Abstract

Microglia, a member of mononuclear phagocyte system, plays a significant role in maintaining homeostasis in central nervous system(CNS). As a subtype of stroke, subarachnoid hemorrhage (SAH)leads to an early brain injury within 72 hours and a delayed brain injury in 3-5 days. Vasospasm used to be regarded as a crucial mechanism of brain injury after subarachnoid hemorrhage, but recently increasing attention is focused on inflammation in brain injury. Microglia polarize to M1 type to act as an pro-inflammatory agent or to M2 type to become a neuro-protector in inflammation in both early stage and delay stage after subarachnoid hemorrhage. Here, we summarize researches on the role of microglia in the brain injury after subarachnoid hemorrhage, to find the research hotspot and provide potential targets for further clinical investigations.

Key words

Subarachnoid hemorrhage / Microglia / Brain injury

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PENG Shu-chen YANG Xiao-mei. Research progress of the role of microglia in the brain injury after subarachnoid hemorrhage[J]. Acta Anatomica Sinica. 2018, 49(4): 556-560 https://doi.org/10.16098/j.issn.0529-1356.2018.04,024

References

［1］ Chen S, Feng H, Sherchan P, et al. Controversies and evolving new mechanisms in subarachnoid hemorrhage［J］. Prog Neurobiol,2014,115:64-91.

［2］ Schneider UC, Davids AM, Brandenburg S, et al. Microglia inflict delayed brain injury after subarachnoid hemorrhage［J］. Acta Neuropathol,2015,130(2):215-231.

［3］ Zheng VZ, Wong GKC. Neuroinflammation responses after subarachnoid hemorrhage: a review［J］. J Clin Neurosci, 2017,42:7-11.

［4］ Naraoka M, Matsuda N, Shimamura N, et al. The role of arterioles and the microcirculation in t he development of vasospasm after aneurysmal SAH ［J］. Biomed Res Int, 2014, 2014:253746.

［5］ Xu HL, Pelligrino DA, Paisansathan C, et al. Protective role of fingolimod (FTY720) in rats subjected to subarachnoid hemorrhage［J］. J Neuroinflammation,2015,12(1):16.

［6］ Schiefecker AJ, Dietmann A, Beer R,et al. Neuroinflammation is associated with brain extracellular tau-protein release after spontaneous subarachnoid hemorrhage［J］. Curr Drug Targets, 2017,18(12): 1408-1416.

［7］ Changyaleket B, Chong ZZ, Dull RO, et al. Heparanase promotes neuroinflammatory response during subarachnoid hemorrhage in rats［J］. J Neuroinflammation, 2017,14(1):137.

［8］ Yang X, Chen C, Hu Q, et al. γ-Secretase inhibitor (GSI1) attenuates morphological cerebral vasospasm in 24h after experimental subarachnoid hemorrhage in rats［J］. Neurosci Lett, 2010,469(3):385-390.

［9］ Lucke-Wold BP, Logsdon AF, Manoranjan B, et al. Aneurysmal subarachnoid hemorrhage and neuroinflammation: a comprehensive review［J］. Int J Mol Sci, 2016,17(12):497.

［10］ van Dijk BJ, Vergouwen MD, Kelfkens MM, et al. Glial cell response after aneurysmal subarachnoid hemorrhage — Functional consequences and clinical implications［J］. Biochim Biophysi Acta,2016,1862(3):492-505.

［11］ Schafer DP, Lehrman EK, Stevens B. The “quad-partite” synapse: microglia-synapse interactions in the developing and mature CNS［J］. Glia,2013,61(1):24-36.

［12］ Liu Y, Zou X, Chai Y, et al. Macrophage polarization in inflammatory diseases［J］. Int J Biol Sci, 2014,10(5):520-529.

［13］ Zhou D, Huang C, Lin Z, et al. Macrophage polarization and function with emphasis on the evolving roles of coordinated regulation of cellular signaling pathways［J］. Cell Signal, 2014,26(2):192-197.

［14］ Sica A, Mantovani A. Macrophage plasticity and polarization: in vivo veritas［J］. J Clin Invest, 2012,122(3):787-795.

［15］ David S, Kroner A. Repertoire of microglial and macrophage responses after spinal cord injury［J］. Nat Rev Neurosci,2011,12(7):388-399.

［16］ Kang K, Reilly SM, Karabacak Ⅴ, et al. Adipocyte-derived Th2 cytokines and myeloid PPAR delta regulate macrophage polarization and insulin sensitivity［J］. Cell Metab,2008,7(6):485-495.

［17］ Mills CD. Anatomy of a discovery: M1 and M2 macrophages［J］. Front Immunol, 2015,6：212.

［18］ Hu X, Li P, Guo Y, et al. Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia［J］. Stroke,2012,43(11):3063-3070.

［19］ Hanafy KA. The role of microglia and the TLR4 pathway in neuronal apoptosis and vasospasm after subarachnoid hemorrhage［J］. J Neuroinflammation,2013,10:83.

［20］ Zhang G, Ghosh S. Toll-like receptor-mediated NF-kappaB activation: a phylogenetically conserved paradigm in innate immunity［J］. J Clin Invest,2001,107(1):13-19.

［21］ Quintana FJ. Old dog, new tricks: IL-6 cluster signaling promotes pathogenic TH17 cell differentiation［J］. Nat Immunol,2016,18(1):8-10.

［22］ Greenhalgh AD, Brough D, Robinson EM, et al. Interleukin-1 receptor antagonist is beneficial after subarachnoid haemorrhage in rat by blocking haem-driven inflammatory pathology［J］. Dis Model Mech,2012,5(6):823-833.

［23］ Wu Y, Pang J, Peng J, et al. An apoE-derived mimic peptide, COG1410, alleviates early brain injury via reducing apoptosis and neuroinflammation in a mouse model of subarachnoid hemorrhage［J］. Neurosci Lett, 2016,627:92-99.

［24］ Li H, Wu W, Sun Q, et al. Expression and cell distribution of receptor for advanced glycation end-products in the rat cortex following experimental subarachnoid hemorrhage［J］. Brain Res,2014,1543:315-323.

［25］ Sun Q, Wu W, Hu Y C, et al. Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro［J］. J Neuroinflammation,2014,11:106.

［26］ Ye Z, Zhuang Z, Wu L, et al. Expression and cell distribution of leukotriene B4 receptor 1 in the rat brain cortex after experimental subarachnoid hemorrhage［J］. Brain Res, 2016,1652:127-134.

［27］ Ayer R, Jadhav Ⅴ, Sugawara T, et al. The neuroprotective effects of cyclooxygenase-2 inhibition in a mouse model of aneurysmal subarachnoid hemorrhage［J］. Acta Neurochir Suppl,2011,111:145-149.

［28］ Aoki T, Frosen J, Fukuda M, et al. Prostaglandin E2-EP2-NF-kappaB signaling in macrophages as a potential therapeutic target for intracranial aneurysms［J］. Sci Signal,2017,10(465):1-17.

［29］ Zhang ZY, Sun BL, Liu JK, et al. Activation of mGluR5 attenuates microglial activation and neuronal apoptosis in early brain injury after experimental subarachnoid hemorrhage in rats［J］. Neurochem Res,2015,40(6):1121-1132.

［30］ Zhang X, Zhang X, Zhang Q, et al. Astaxanthin reduces matrix metalloproteinase-9 expression and activity in the brain after experimental subarachnoid hemorrhage in rats［J］. Brain Res,2015,1624:113-124.

［31］ Schallner N, Pandit R, Leblanc RR, et al. Microglia regulate blood clearance in subarachnoid hemorrhage by heme oxygenase-1［J］. J Clin Invest,2015,125(7):2609-2625.

［32］ Kooijman E, Nijboer CH, van Velthoven CT, et al. Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat［J］. PLoS One,2014,9(6):e90584.

［33］ Zhang T, Su J, Guo B, et al. Apigenin protects blood-brain barrier and ameliorates early brain injury by inhibiting TLR4-mediated inflammatory pathway in subarachnoid hemorrhage rats［J］. Int Immunopharmacol, 2015,28(1):79-87.

［34］ Xie Z, Huang L, Enkhjargal B, et al. Recombinant Netrin-1 binding UNC5B receptor attenuates neuroinflammation and brain injury via PPARγ/NFκB signaling pathway after subarachnoid hemorrhage in rats［J］. Brain Behav Immun, 2017，69:190-202.

［35］ Fang R, Zheng X, Zhang M. Ethyl pyruvate alleviates early brain injury following subarachnoid hemorrhage in rats［J］. Acta Neurochir (Wien),2016,158(6):1069-1076.

［36］ Zhang ZY, Sun BL, Yang MF, et al. Carnosine attenuates early brain injury through its antioxidative and anti-apoptotic effects in a rat experimental subarachnoid hemorrhage model［J］. Cell Mol Neurobiol,2015，35（2）：147-157.

［37］ Kotlega D, Golab-Janowska M, Masztalewicz M, et al. Potential role of statins in the intracerebral hemorrhage and subarachnoid hemorrhage［J］. Neurol Neurochir Pol,2015,49(5):322-328.

［38］ Chen T, Wang W, Li J, et al. PARP inhibition attenuates early brain injury through NF-κB /MMP-9 pathway in a rat model of subarachnoid hemorrhage［J］. Brain Res, 2016, 1644:32-38.

［39］ You W, Wang Z, Li H, et al. Inhibition of mammalian target of rapamycin attenuates early brain injury through modulating microglial polarization after experimental subarachnoid hemorrhage in rats［J］. J Neurol Sci,2016,367:224-231.

［40］ Hao G, Dong Y, Huo R, et al. Rutin inhibits neuroinflammation and provides neuroprotection in an experimental rat model of subarachnoid hemorrhage, possibly through suppressing the RAGE-NF-κB inflammatory signaling pathway［J］. Neurochem Res, 2016, 41(6):1496-1504.