Phagocytic microglia and macrophages in brain injury and repair

Yu, Fang; Wang, Yangfan; Stetler, Anne R; Leak, Rehana K.; Hu, Xiaoming

doi:10.1111/cns.13899

Cited by 85 publications

(47 citation statements)

References 186 publications

(475 reference statements)

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“…Shi et al reported that the function of Treg cells in facilitating oligodendrogenesis and remyelination was mediated by promoting tissue‐reparative microglia responses following crosstalk with microglia at the chronic stage of stroke 86 . It was reported that ischemic postconditioning (reperfusion for 10 min after which the middle cerebral artery was reoccluded for 10 min) for one episode can facilitate to shift microglia into tissue repairing forms, 52 which actively participate in myelin repair 87,88 . In addition, a recent study confirmed the contribution of RIC is linked to Treg cells thriving.…”

Section: Evaluation Of the Hypothesismentioning

confidence: 94%

A review of remote ischemic conditioning as a potential strategy for neural repair poststroke

Ren

2022

CNS Neurosci Ther

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Ischemic stroke is one of the major disabling health‐care problem and multiple different approaches are needed to enhance rehabilitation, in which neural repair is the structural basement. Remote ischemic conditioning (RIC) is a strategy to trigger endogenous protect. RIC has been reported to play neuroprotective role in acute stage of stroke, but the effect of RIC on repair process remaining unclear. Several studies have discovered some overlapped mechanisms RIC and neural repair performs. This review provides a hypothesis that RIC is a potential therapeutic strategy on stroke rehabilitation by evaluating the existing evidence and puts forward some remaining questions to clarify and future researches to be performed in the field.

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Section: Evaluation Of the Hypothesismentioning

confidence: 94%

A review of remote ischemic conditioning as a potential strategy for neural repair poststroke

Ren

2022

CNS Neurosci Ther

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“…Microglia also can engulf infiltrating immune cells in the injured brain and modulate their pro-inflammatory properties (Yu et al, 2022 ). Microglia clear granulocytes within 24 h after ischemia insults to attenuate apoptosis of neurons (Neumann et al, 2008 ).…”

Section: Microglial Crosstalk With Other Cellular Brain Partnersmentioning

confidence: 99%

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Wang

Leak

Cao

2022

Front. Cell. Neurosci.

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Stroke remains a major cause of long-term disability and mortality worldwide. The immune system plays an important role in determining the condition of the brain following stroke. As the resident innate immune cells of the central nervous system, microglia are the primary responders in a defense network covering the entire brain parenchyma, and exert various functions depending on dynamic communications with neurons, astrocytes, and other neighboring cells under both physiological or pathological conditions. Microglia activation and polarization is crucial for brain damage and repair following ischemic stroke, and is considered a double-edged sword for neurological recovery. Microglia can exist in pro-inflammatory states and promote secondary brain damage, but they can also secrete anti-inflammatory cytokines and neurotrophic factors and facilitate recovery following stroke. In this review, we focus on the role and mechanisms of microglia-mediated neuroinflammation and neuroplasticity after ischemia and relevant potential microglia-based interventions for stroke therapy.

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“…Through both M1 and M2 microglia own phagocytic receptors, the M2 phenotype has higher phagocytic capabilities to clear dead neurons than the M1 phenotype 52 . The M1 phenotype inaccurately engulfs normal neurons, while the M2 phenotype has neuroprotection through antioxidant functions 53 …”

Section: Introductionmentioning

confidence: 99%

“… 52 The M1 phenotype inaccurately engulfs normal neurons, while the M2 phenotype has neuroprotection through antioxidant functions. 53 …”

Section: Introductionmentioning

confidence: 99%

“…52 The M1 phenotype inaccurately engulfs normal neurons, while the M2 phenotype has neuroprotection through antioxidant functions. 53 Sex has been gradually recognized as a vital biological variable in the treatment of neurodegenerative disorders (such as stroke) and sexually dimorphic microglia are potential targets. 54 There are remarkabe differences between microglia and neuro-immune signaling in the male and female brain during the whole life, and these differences may facilitate a huge difference in the process and repair of CNS damage and neurodegeneration.…”

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confidence: 99%

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NG2‐glia crosstalk with microglia in health and disease

Zuo

Zhou

et al. 2022

CNS Neurosci Ther

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Glia are non-neuronal cells, also called neuroglia. 1 Glia exist within the mammalian nervous system to provide several essential functions for neurons, such as maintaining homeostasis, support, protection, and generating myelin. 2,3 Traditionally, astrocytes, microglia, and oligodendrocytes are the three major classes of glia. In the last two decades, neuron glia antigen-2 (NG2) glial cell has been considered as the fourth type of glial cell in the central nervous system (CNS). 4 NG2-glia are also called oligodendrocyte precursor cells 5 and express NG2. [6][7][8] NG2 is a chondroitin sulphate proteoglycan 4 (CSPG4), which is also expressed on infiltrating macrophages and activated microglia in various CNS insults. 9-11 NG2, together with platelet-derived growth factor receptor alpha (PDGFRα), is a marker of NG2-glia. 12,13 NG2-glia account for 5%-10% of all cells in the adult CNS. 14 NG2-glia are extremely heterogeneous with different characteristics and functions. 15,16 NG2-glia are widely scattered in the CNS in late development and throughout adulthood. NG2-glia may differentiate into neurons or astrocytes under diverse conditions, such as at embryonic stages, and under forced expression of neurogenic factors. [17][18][19] Early postnatal NG2-glia can become multipotent neurospheres and quickly differentiate into neurons, astrocytes, and oligodendrocytes in vitro. 18 More than one-third of the protoplasmic astrocytes are differentiated from NG2-glia in ventral forebrain when NG2-Cre is prenatally triggered in NG2-glia before embryonic day 17.5. 20 A single homeodomain transcription factor Dlx2-transfects NG2-glia differentiated into GABAergic inhibitory neurons. 19 Adult NG2-glia also differentiate into neurons in the cortical gray matter. 21 The anti-epileptic epigenetic regulator valproic

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Phagocytic microglia and macrophages in brain injury and repair

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 85 publications

References 186 publications

A review of remote ischemic conditioning as a potential strategy for neural repair poststroke

A review of remote ischemic conditioning as a potential strategy for neural repair poststroke

Microglia-mediated neuroinflammation and neuroplasticity after stroke

NG2‐glia crosstalk with microglia in health and disease

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