Microglial-produced nitric oxide and reactive nitrogen oxides mediate neuronal cell death

Boje, Kathleen M. K.; Arora, Prince K.

doi:10.1016/0006-8993(92)91004-x

Cited by 906 publications

(547 citation statements)

References 44 publications

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“…The toxicity originates from in vitro studies that demonstrated neuronal survival is attenuated by exposure to both microglia treated with proinflammatory stimuli and the supernatant of the treated microglia [49,50]. These activated microglia release cytotoxic factors such as superoxide, nitric oxide, and tumor necrosis factor (TNF)-α [51][52][53][54][55].…”

Section: Microgliamentioning

confidence: 99%

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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Historically, the brain has been considered an immune-privileged organ separated from the peripheral immune system by the blood-brain barrier. However, immune responses do occur in the brain in neurological conditions in which the integrity of the blood-brain barrier is compromised, exposing the brain to peripheral antigens and endogenous danger signals. While most of the associated pathological processes occur in the central nervous system, it is now clear that peripheral immune cells, especially mononuclear phagocytes, that infiltrate into the injury site play a key role in modulating the progression of primary brain injury development. As inflammation is a necessary and critical component for the subsequent injury resolution process, understanding the contribution of mononuclear phagocytes on the regulation of inflammatory responses may provide novel approaches for potential therapies. Furthermore, predisposed comorbid conditions at the time of stroke cause the alteration of stroke-induced immune and inflammatory responses and subsequently influence stroke outcome. In this review, we summarize a role for microglia and monocytes/macrophages in acute ischemic stroke in the context of normal and metabolically compromised conditions.

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Section: Microgliamentioning

confidence: 99%

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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“…For example, it has been shown that high levels of NO derived from microglia stimulated with LPS induced neuronal death by inhibition of neuronal respiration. NO inhibition of neuronal respiration caused, in turn, neuronal depolarization and glutamate release, followed by excitotoxicity via the NMDA receptor [103-106]. Accordingly, NMDA receptor-mediated toxicity towards cerebellar granule neurons was potentiated by co-culture with immunostimulated microglia or by co-exposure to an NO donor [107].…”

Section: Nitric Oxide In the Cross-talk Between Microglia And Neuronsmentioning

confidence: 99%

Neuronal-glial Interactions Define the Role of Nitric Oxide in Neural Functional Processes

Contestabile¹,

Monti²,

Polazzi³

2012

Current Neuropharmacology

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Nitric oxide (NO) is a versatile cellular messenger performing a variety of physiologic and pathologic actions in most tissues. It is particularly important in the nervous system, where it is involved in multiple functions, as well as in neuropathology, when produced in excess. Several of these functions are based on interactions between NO produced by neurons and NO produced by glial cells, mainly astrocytes and microglia. The present paper briefly reviews some of these interactions, in particular those involved in metabolic regulation, control of cerebral blood flow, axonogenesis, synaptic function and neurogenesis. Aim of the paper is mainly to underline the physiologic aspects of these interactions rather than the pathologic ones.

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“…These include the cytokines tumor necrosis factor-␣ (TNF␣) and interleukin-1␤ (IL-1␤), free radicals such as nitric oxide (NO) and superoxide, fatty acid metabolites such as eicosanoids, and quinolinic acid. Studies using cell culture and animal models have demonstrated that excessive quantities of individual factors produced by activated microglia can be deleterious to neurons (Boje and Arora, 1992;Chao et al, 1992;McGuire et al, 2001). Furthermore, individual factors often work in concert to induce neurodegeneration.…”

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confidence: 99%