The effect of norepinephrine on endotoxin-mediated macrophage activation

Hu, Xiaoxi; Goldmuntz, Ellen A.; Brosnan, Celia F.

doi:10.1016/0165-5728(91)90084-k

Cited by 110 publications

(43 citation statements)

References 27 publications

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“…5,6 The central nervous system modulates systemic inflammatory responses to various stressors through humoral mechanisms. [7][8][9] Stimulation of afferent vagus nerve fibers by cytokines or endotoxin stimulates pituitary-adrenal antiinflammatory responses 10 -12 ; however, a role of efferent vagus nerve signaling also exists in modulating inflammation.…”

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confidence: 99%

Efferent Vagal Fibre Stimulation Blunts Nuclear Factor-κB Activation and Protects Against Hypovolemic Hemorrhagic Shock

et al. 2003

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confidence: 99%

Efferent Vagal Fibre Stimulation Blunts Nuclear Factor-κB Activation and Protects Against Hypovolemic Hemorrhagic Shock

et al. 2003

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“…Extrasynaptic NA is thought to execute additional functions apart from its role as classical neurotransmitter. NA blocks the expression of inflammation-induced proteins, including major histocompatibility complex class II (Frohman et al, 1988), tumor necrosis factor-␣ (Hu et al, 1991), interleukin-1␤ (IL-1␤) (Willis and Nisen, 1995), and inducible nitric oxide synthase (iNOS) in astrocytes and microglia . In vivo noradren-dsp4 the animals received fluoxetine (10 mg/kg) to protect serotonergic fibers, thereby increasing the selectivity of dsp4 for noradrenergic neurons.…”

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confidence: 99%

Locus Ceruleus Degeneration Promotes Alzheimer Pathogenesis in Amyloid Precursor Protein 23 Transgenic Mice

et al. 2006

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Locus ceruleus (LC) degeneration and loss of cortical noradrenergic innervation occur early in Alzheimer's disease (AD). Although this has been known for several decades, the contribution of LC degeneration to AD pathogenesis remains unclear. We induced LC degeneration with N-(2-chloroethyl)-N-ethyl-bromo-benzylamine (dsp4) in amyloid precursor protein 23 (APP23) transgenic mice with a low amyloid load. Then 6 months later the LC projection areas showed a robust elevation of glial inflammation along with augmented amyloid plaque deposits. Moreover, neurodegeneration and neuronal loss significantly increased. Importantly, the paraventricular thalamus, a nonprojection area, remained unaffected. Radial arm maze and social partner recognition tests revealed increased memory deficits while high-resolution magnetic resonance imaging-guided micro-positron emission tomography demonstrated reduced cerebral glucose metabolism, disturbed neuronal integrity, and attenuated acetylcholinesterase activity. Nontransgenic mice with LC degeneration were devoid of these alterations. Our data demonstrate that the degeneration of LC affects morphology, metabolism, and function of amyloid plaque-containing higher brain regions in APP23 mice. We postulate that LC degeneration substantially contributes to AD development.

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“…In microglial cells, induction of tumor necrosis factor-ct (TNF-cr) synthesis by LPS can be blocked by norepinephrine (NE) (Hu et al, 1991), whereas in astrocyte cultures, interferon-y (IFN-y)-induced expression of class II antigens is decreased by NE (Frohman et al, 1988), and LPS induction of ILl-‚8 expression is suppressed by dibutyryl cyclic AMP (dbcAMP) (Willis and Nisen, 1995). These observaIn brain, inflammatory responses of glial cells occur during disease, infection, and ischemia.…”

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confidence: 99%

Suppression of Astroglial Nitric Oxide Synthase Expression by Norepinephrine Results from Decreased NOS‐2 Promoter Activity

Feinstein

1998

Journal of Neurochemistry

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Abstract:We previously demonstrated that norepinephrifle (NE) inhibits induction of the calcium-independent isoform of nitric oxide synthase (NOS-2) in primary rat astrocyte cultures. However, the molecular mechanisms underlying this effect are unknown. In C6 cells and astrocytes, NE suppressed both cytokine-and lipopolysaccharide (LPS)-dependent nitrite accumulation, an index of NOS-2 activity. NE reduced the steady-state levels of NOS-2 mRNA induced by LPS plus cytokines but did not decrease NOS-2 mRNA stability or inhibit activation or subunit composition of transcription factor nuclear factor KB, which is necessary for NOS-2 induction. In 06 cells stably transfected with a 1 ‚588-bp mouse NOS-2 promoter, NE reduced LPS plus cytokine-induced reporter gene expression, suggesting inhibition of NOS-2 promoter activity. In contrast, suppression was lost when a truncated 85-bp NOS-2 promoter was used, and in these cells NE potentiated reporter gene expression, alone or in the presence of LPS and cytokines. These results suggest that the suppressive effects of NE are due to modification of transcription factor activity in a region located between -1,588 and -85 of the NOS-2 promoter and may help explain observations that in some cells cyclic AMP can potentiate, rather than suppress, NOS-2 expression.

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The effect of norepinephrine on endotoxin-mediated macrophage activation

Cited by 110 publications

References 27 publications

Efferent Vagal Fibre Stimulation Blunts Nuclear Factor-κB Activation and Protects Against Hypovolemic Hemorrhagic Shock

Efferent Vagal Fibre Stimulation Blunts Nuclear Factor-κB Activation and Protects Against Hypovolemic Hemorrhagic Shock

Locus Ceruleus Degeneration Promotes Alzheimer Pathogenesis in Amyloid Precursor Protein 23 Transgenic Mice

Suppression of Astroglial Nitric Oxide Synthase Expression by Norepinephrine Results from Decreased NOS‐2 Promoter Activity

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