Anti-inflammatory effects of noradrenaline on LPS-treated microglial cells: Suppression of NFκB nuclear translocation and subsequent STAT1 phosphorylation

Ishii, Yurika; Yamaizumi, Ayaka; Kawakami, Ayu; Islam, Afsana; Choudhury, Mohammed E.; Takahashi, Hiroyuki; Yano, Hajime; Tanaka, Junya

doi:10.1016/j.neuint.2015.07.010

Cited by 46 publications

(51 citation statements)

References 43 publications

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“…Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) is another important signaling molecule that plays a key role in induction of pro-inflammatory cytokines and chemokines in microglia and macrophages [25,26]. We confirmed that CAPE (10 μM), an inhibitor of NF-κB [27], virtually abolished LPS-induced CXCL2 mRNA expression in BV-2 cells (Fig.…”

Section: Am80 Suppresses Nf-κb Signalingsupporting

confidence: 62%

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Retinoic acid receptor agonist Am80 inhibits CXCL2 production from microglial BV-2 cells via attenuation of NF-κB signaling

Takaoka

Takahashi

Kurauchi

et al. 2016

International Immunopharmacology

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Section: Am80 Suppresses Nf-κb Signalingsupporting

confidence: 62%

“…NF-κB is another important signaling component downstream of TLRs that triggers expression of pro-inflammatory cytokines and chemokines [25,26]. The most notable finding in the present study is that regulation of NF-κB signaling pathway may play a key role in the anti-inflammatory effect of RAR stimulation.…”

Section: Discussionsupporting

confidence: 49%

Retinoic acid receptor agonist Am80 inhibits CXCL2 production from microglial BV-2 cells via attenuation of NF-κB signaling

Takaoka

Takahashi

Kurauchi

et al. 2016

International Immunopharmacology

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“…The 6‐hr delay of the light‐on and ‐off timing caused a 6‐hr delay of circadian expressional changes in microglial markers and NA content fluctuation, suggesting a linkage between microglial and neuronal activities. Circadian changes in LC‐derived NA contents in the brain (Aston‐Jones & Bloom, ) and the suppressive effects of NA on microglia are well‐known (Ishii et al, ; Mori et al, ). Glu enhances phagocytic activity of primary cultured rat microglia (Aono et al, ), and NA overcomes the Glu‐induced enhancement, as was shown in the present study.…”

Section: Discussionmentioning

confidence: 99%

Phagocytic elimination of synapses by microglia during sleep

Choudhury

Miyanishi

Tamano

et al. 2019

Glia

Self Cite

107

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Synaptic strength reduces during sleep, but the underlying mechanisms of this process are unclear. This study showed reduction of synaptic proteins in rat prefrontal cortex (PFC) at AM7 or Zeitgeber Time (ZT0), when the light phase or sleeping period for rats started. At this time point, microglia were weakly activated, displaying larger and more granular somata with increased CD11b expression compared with those at ZT12, as revealed by flow cytometry. Expression of opsonins, such as complements or MFG‐E8, matrix metalloproteinases, and microglial markers at ZT0 were increased compared with that at ZT12. Microglia at ZT0 phagocytosed synapses, as revealed by immunohistochemical staining. Immunoblotting detected more synapsin I in the isolated microglia at ZT0 than at ZT12. Complement C3‐ or MFG‐E8‐bound synapses were the most abundant at ZT0, some of which were phagocytosed by microglia. Systemic administration of synthetic glucocorticoid dexamethasone reduced microglial size, granularity and CD11b expression at ZT0, resembling microglia at ZT12, and increased synaptic proteins and decreased the sleeping period. Noradrenaline (NA) suppressed glutamate‐induced phagocytosis in primary cultured microglia. Systemic administration of the brain monoamine‐depleting agent reserpine decreased NA content and synapsin I expression in PFC, and increased expression of microglia markers, C3 and MFG‐E8, while increasing the sleeping period. A NA precursor l‐threo‐dihydroxyphenylserine abolished the reserpine‐induced changes. These results suggest that microglia may eliminate presumably weak synapses during every sleep phase. The circadian changes in concentrations of circulating glucocorticoids and brain NA might be correlated with the circadian changes of microglial phenotypes and synaptic strength.

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“…); and more recently in primary microglial cells (Ishii et al . ). In vivo studies showed that NA depletion using the selective neurotoxin N ‐(2‐chloroethyl)‐ N ‐ethyl‐2‐bromobenzylamine (DSP4) to destroy NA producing cells increased inflammatory responses (Heneka et al .…”

Section: Na Actions Involve Suppression Of Nfκbmentioning

confidence: 97%

Causes, consequences, and cures for neuroinflammation mediated via the locus coeruleus: noradrenergic signaling system

Feinstein

Kalinin

Braun

2016

Journal of Neurochemistry

140

128

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Aside from its roles in as a classical neurotransmitter involved in regulation of behavior, noradrenaline (NA) has other functions in the CNS. This includes restricting the development of neuroinflammatory activation, providing neurotrophic support to neurons, and providing neuroprotection against oxidative stress. In recent years, it has become evident that disruption of physiological NA levels or signaling is a contributing factor to a variety of neurological diseases and conditions including Alzheimer's disease (AD) and Multiple Sclerosis. The basis for dysregulation in these diseases is, in many cases, due to damage occurring to noradrenergic neurons present in the locus coeruleus (LC), the major source of NA in the CNS. LC damage is present in AD, multiple sclerosis, and a large number of other diseases and conditions. Studies using animal models have shown that experimentally induced lesion of LC neurons exacerbates neuropathology while treatments to compensate for NA depletion, or to reduce LC neuronal damage, provide benefit. In this review, we will summarize the anti-inflammatory and neuroprotective actions of NA, summarize examples of how LC damage worsens disease, and discuss several approaches taken to treat or prevent reductions in NA levels and LC neuronal damage. Further understanding of these events will be of value for the development of treatments for AD, multiple sclerosis, and other diseases and conditions having a neuroinflammatory component.

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Anti-inflammatory effects of noradrenaline on LPS-treated microglial cells: Suppression of NFκB nuclear translocation and subsequent STAT1 phosphorylation

Cited by 46 publications

References 43 publications

Retinoic acid receptor agonist Am80 inhibits CXCL2 production from microglial BV-2 cells via attenuation of NF-κB signaling

Retinoic acid receptor agonist Am80 inhibits CXCL2 production from microglial BV-2 cells via attenuation of NF-κB signaling

Phagocytic elimination of synapses by microglia during sleep

Causes, consequences, and cures for neuroinflammation mediated via the locus coeruleus: noradrenergic signaling system

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