Ephrin‐A3 and Ephrin‐A4 Contribute to Microglia‐Induced Angiogenesis in Brain Endothelial Cells

Liu, Ying; Liu, Dongxin; Li, Mei-Yang; Qin, Xiaoxue; Fang, Wen-Gang; Zhao, Wei‐Dong; Chen, Yuhua

doi:10.1002/ar.22998

Cited by 28 publications

(18 citation statements)

References 44 publications

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“…Some other factors secreted by microglia, such as protease serine 2, brain-derived neurotrophic factor, and glial cell line-derived neurotrophic factor, can also promote neurogenesis [98]. Furthermore, microglia upregulate endothelial ephrin-A3 and ephrin-A4 expression to facilitate in vitro angiogenesis of brain endothelial cells [99]. These studies provide evidence that microglia may promote neurogenesis and angiogenesis, which are beneficial for brain function recovery.…”

Section: Microgliamentioning

confidence: 99%

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

et al. 2016

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Intracerebral hemorrhage (ICH) is a subtype of stroke with high mortality and morbidity. When a diseased artery within the brain bursts, expansion and absorption of the resulting hematoma trigger a series of reactions that cause primary and secondary brain injury. Microglia are extremely important for removing the hematoma and clearing debris, but they are also a source of ongoing inflammation. This article discusses the role of microglial activation/polarization and related inflammatory mediators, such as Toll-like receptor 4, matrix metalloproteinases, high-mobility group protein box-1, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron, in secondary injury after ICH and highlights the potential targets for ICH treatment.

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Section: Microgliamentioning

confidence: 99%

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

et al. 2016

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“…In primary rat cerebral endothelial cultures, TNFα potently increased EPO receptor expression; further exposure to EPO in TNFα-treated cells significantly promoted matrigel tube formation, whereas blocking TNFR1 dampened TNFα-induced EPO receptor levels and prevented EPO-induced tube formation (Wang et al 2011b). Recently, it has been proposed that microglia enhanced in vitro angiogenesis of brain microvascular endothelial cells by releasing TNFα and upregulating the expression of angiogenic factors ephrin-A3 and ephrin-A4 (Li et al 2014). Altogether, these data are consistent with the idea that TNFα may act as a remodeling signal within the recovering neurovascular unit.…”

Section: Extracellular Signals Within the Neurovascular Unit For Nmentioning

confidence: 99%

Help-me signaling: Non-cell autonomous mechanisms of neuroprotection and neurorecovery

Xing

2017

Progress in Neurobiology

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Self-preservation is required for life. At the cellular level, this fundamental principle is expressed in the form of molecular mechanisms for preconditioning and tolerance. When the cell is threatened, internal cascades of survival signaling become triggered to protect against cell death and defend against future insults. Recently, however, emerging findings suggest that this principle of self-preservation may involve not only intracellular signals; the release of extracellular signals may provide a way to recruit adjacent cells into an amplified protective program. In the central nervous system where multiple cell types co-exist, this mechanism would allow threatened neurons to “ask for help” from glial and vascular compartments. In this review, we describe this new concept of help-me signaling, wherein damaged or diseased neurons release signals that may shift glial and vascular cells into potentially beneficial phenotypes, and help remodel the neurovascular unit. Understanding and dissecting these non-cell autonomous mechanisms of self-preservation in the CNS may lead to novel opportunities for neuroprotection and neurorecovery.

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“…Recent studies suggested that microglia regulate vascular branching and proliferation via release of soluble mediators which either promote or inhibit vascular network formation (Arnold and Betsholtz, 2013; Stefater et al, 2011). More recently, microglia have been shown to facilitate angiogenesis in vitro via release of tumor necrosis factor-α (TNF-α), which upregulates endothelial ephrin-A3 and ephrin-A4 (Li et al, 2014). Moreover, microglia are endowed with neurotransmitter receptors including iono-and metabo-tropic Glu receptors (Pocock and Kettenmann, 2007) and are reactive to neural activity (Hung et al, 2010; Wake et al, 2009).…”

Section: Possible Mechanisms Underlying Activity-induced Cerebrovmentioning

confidence: 99%

Control of cerebrovascular patterning by neural activity during postnatal development

Lacoste

2015

Mechanisms of Development

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The brain represents only a small portion of the body mass and yet consumes almost a quarter of the available energy, and has a limited ability to store energy. The brain is therefore highly dependent on oxygen and nutrient supply from the blood circulation, which makes it vulnerable to vascular pathologies. Key vascular determinants will ensure proper brain maturation and function: the establishment of vascular networks, the formation of the blood-brain barrier, and the regulation of blood flow. Recent evidence suggests that the phenomenon of neurovascular coupling, during which increased neural activity normally leads to increased blood flow, is not functional until few weeks after birth, implying that the developing brain must rely on alternative mechanisms to adequately couple blood supply to increasing energy demands. This review will focus on these alternative mechanisms, which have been partly elucidated recently via the demonstration that neural activity influences the maturation of cerebrovascular networks. We also propose possible mechanisms underlying activity-induced vascular plasticity.

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Ephrin‐A3 and Ephrin‐A4 Contribute to Microglia‐Induced Angiogenesis in Brain Endothelial Cells

Cited by 28 publications

References 44 publications

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

Help-me signaling: Non-cell autonomous mechanisms of neuroprotection and neurorecovery

Control of cerebrovascular patterning by neural activity during postnatal development

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