Histamine production by cultured microglial cells of the mouse

Katoh, Yoshiko; Niimi, Mitsuhiro; Yamamoto, Yumiko; Kawamura, Tomohiro; Morimoto-Ishizuka, Tomoko; Sawada, Makoto; Takemori, Hiroshi; Yamatodani, Atsushi

doi:10.1016/s0304-3940(01)01835-3

Cited by 69 publications

(40 citation statements)

References 18 publications

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“…This would support the hypothesis that pharmacological targeting of histamine receptors is an appropriate diseasemodifying therapeutic approach against neuroinflammatory and autoimmune diseases [8,9]. Among several inflammatory mediators, rat and mouse microglia appears sensitive to histamine challenge [10][11][12]. Recent work has identified the expression of histamine receptors, particularly H1, on microglial N9 cell line [13] and rat primary microglia [14].…”

Section: Introductionsupporting

confidence: 52%

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

et al. 2014

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Mutations in the Cu(2+)/Zn(2+) superoxide dismutase 1 (SOD1) gene underlie 14-23 % of familial and 1-7 % of sporadic cases of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease characterized by a specific loss of motor neurons in the brain and spinal cord. Neuroinflammation and oxidative stress are emerging as key players in the pathogenesis of ALS, thus justifying the interest in glial cells and particularly microglia, in addition to motor neurons, as novel therapeutic approaches against ALS. Recently, histamine was proven to participate in the pathogenesis of neuroinflammatory and neurodegenerative diseases, and particularly, microglia was shown to be sensitive to the histamine challenge mainly through histamine H1 receptors. Clemastine is a first-generation and CNS-penetrant H1 receptor antagonist considered as a safe antihistamine compound that was shown to possess immune suppressive properties. In order to investigate if clemastine might find promising application in the treatment of ALS, in this work, we tested its action in the SOD1(G93A) mouse model which is extensively used in ALS preclinical studies. We demonstrated that chronic clemastine administration in SOD1(G93A) mice reduces microgliosis, modulates microglia-related inflammatory genes, and enhances motor neuron survival. Moreover, in vitro, clemastine is able to modify several activation parameters of SOD1(G93A) microglia, and particularly CD68 and arginase-1 expression, as well as phospho-ERK1/2 and NADPH oxidase 2 levels. Being clemastine a drug already employed in clinical practice, our results strongly encourage its further exploitation as a candidate for preclinical trials and a new modulator of neuroinflammation in ALS.

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Section: Introductionsupporting

confidence: 52%

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

et al. 2014

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“…The increased fiber density did not involve the noradrenergic and/or dopaminergic fibers in general, but was specific for the histaminergic system, as a simultaneous decrease and not an increase in tyrosine hydroxylaseimmunoreactive fiber density was detected. Microglial cells might synthesize histamine upon stimulation (Katoh et al, 2001), but visualization of activated microglia and histaminergic fibers revealed that the morphology of activated microglia was different from those structures that we suggested to be swollen fibers with very large varicosities 4 weeks after KA injection, and no histamine-immunoreactivity was detected in activated microglia. Furthermore, very few activated microglia were present at the later time points of increased histaminergic fiber density in the piriform cortex (1 week-4 weeks).…”

Section: Altered Histaminergic Projections In the Piriform Cortical Acontrasting

confidence: 67%

Transient changes in the limbic histaminergic system after systemic kainic acid-induced seizures

Lintunen

Sallmén

Karlstedt

et al. 2005

Neurobiology of Disease

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“…The possibility that ranitidine might act through other receptors besides HA-H 2 could not be excluded. 21 It is also possible that HA released from microglia or astroglia 22 during OGD could directly potentiate glutamate receptor-mediated cell death by interacting with the polyamine-binding site of the NMDA receptor complex. 8 Ranitidine could then be able to antagonize HA interaction with NMDA receptors.…”

Section: Discussionmentioning

confidence: 99%

Histamine H ₂ -Receptor Antagonist Ranitidine Protects Against Neural Death Induced by Oxygen-Glucose Deprivation

Malagelada

Xifró

Badiola

et al. 2004

Stroke

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Background and Purpose-Administration of histamine receptor antagonists has been reported to produce contradictory results, either reducing or increasing neural damage induced by ischemia. In this study, we investigated the neuroprotective effects of histamine H 2 -receptor antagonists in an "in vitro" model of ischemia. Methods-Cultured rat brain cortical neurons were exposed to oxygen-glucose deprivation (OGD) in the presence or absence of different histaminergic drugs. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction assay. Necrosis and apoptosis were quantified by staining cells with propidium iodide and Hoechst 33258. Caspase 3 activation was determined by immunocytochemistry and Western blot. Results-Pretreatment with H 2 antagonists effectively reduced neuronal cell death induced by OGD. Ranitidine decreased the number of necrotic and apoptotic cells. Caspase 3 activation and alteration of the neuronal cytoskeleton were also prevented by ranitidine pretreatment. The neuroprotective effect of ranitidine was still evident when added 6 hours after OGD. Conclusions-H 2 -receptor antagonists protected against OGD-induced neuronal death. Ranitidine attenuated cell death even when administered after OGD. These data suggest that this drug, which is currently used for the treatment of gastric ulcers, may be useful in promoting recovery after ischemia.

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Histamine production by cultured microglial cells of the mouse

Cited by 69 publications

References 18 publications

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

Transient changes in the limbic histaminergic system after systemic kainic acid-induced seizures

Histamine H ₂ -Receptor Antagonist Ranitidine Protects Against Neural Death Induced by Oxygen-Glucose Deprivation

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Histamine production by cultured microglial cells of the mouse

Cited by 69 publications

References 18 publications

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

Transient changes in the limbic histaminergic system after systemic kainic acid-induced seizures

Histamine H 2 -Receptor Antagonist Ranitidine Protects Against Neural Death Induced by Oxygen-Glucose Deprivation

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Histamine H ₂ -Receptor Antagonist Ranitidine Protects Against Neural Death Induced by Oxygen-Glucose Deprivation