Activation of cultured astrocytes by amphotericin B: Stimulation of NO and cytokines production and changes in neurotrophic factors production

Motoyoshi-Yamashiro, Akiko; Tamura, Miki; Moriyama, Mitsuaki; Takano, Katsura; Kawabe, Kentaro; Nakajima, Hidemitsu; Katoh‐Semba, Ritsuko; Furuichi, Teiichi; Nakamura, Yoichi

doi:10.1016/j.neuint.2013.05.007

Cited by 6 publications

(7 citation statements)

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“…Effects of AmB on glial activation : We had previously reported in cultured microglia [20] and astrocytes [21] that AmB could stimulate NO production and change the expression levels of mRNAs of proinflammatory cytokines and neurotrophic factors. To investigate the effects of AmB on glial activation in vivo , we observed the expression of GFAP, an astrocyte marker, and CD11b, a microglial marker, by immunohistochemical analysis after AmB injection.…”

Section: Resultsmentioning

confidence: 99%

“…In an in vitro study, we previously reported that AmB changed the expression of neurotrophic factors in astrocytes [21] and microglia [20]. In AmB-stimulated astrocytes, the expression levels of both BDNF and GDNF proteins were significantly upregulated, and the cellular amounts of neurotrophin-3 protein decreased [21].…”

Section: Discussionmentioning

confidence: 99%

“…In AmB-stimulated astrocytes, the expression levels of both BDNF and GDNF proteins were significantly upregulated, and the cellular amounts of neurotrophin-3 protein decreased [21]. Also, in microglia, AmB stimulation increased the expression levels of BDNF and GDNF mRNAs [20].…”

Section: Discussionmentioning

confidence: 99%

“…In our attempt to elucidate the therapeutic mechanisms of AmB in prion diseases, we previously reported that AmB increased levels of GDNF mRNA in microglia and protein levels of BDNF and GDNF in astrocytes [20, 21]. In the present study, we investigated whether AmB affected glial activation and neurotrophic factor production in vivo .…”

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confidence: 92%

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Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat　Brain

Motoyoshi-Yamashiro

Takano

Kawabe

et al. 2014

The Journal of Veterinary Medical Science

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Amphotericin B (AmB) is a polyene antifungal drug and is reported to be one of a few reagents having therapeutic effects on prion diseases, that is, a delay in the appearance of clinical signs and prolongation of the survival time in an animal model. In prion diseases, glial cells have been suggested to play important roles; however, the therapeutic mechanism of AmB on prion diseases remains elusive. We have previously reported that AmB changed the expression of neurotrophic factors in microglia and astrocytes (Motoyoshi et al., 2008, Neurochem. Int. 52, 1290–1296; Motoyoshi-Yamashiro et al., 2013, ibid. 63, 93–100). These results suggested that neurotrophic factors derived from glial cells might be involved in the therapeutic mechanism of AmB. In the present study, we examined immunohistochemically the effects of AmB on the expression of neurotrophic factors in the rat brain. We found that direct injection of AmB into the striatum significantly enhanced the expression of glial cell line-derived neurotrophic factor protein. Amphotericin B also increased the expressions of CD11b and glial fibrillary acidic protein, markers of microglia and astrocytes, respectively. Moreover, expressions of the two neurotrophic factors by AmB were co-localized with the expression of CD11b or glial fibrillary acidic protein. These results suggest that AmB in vivo might also activate glial cells and induce the production of neurotrophic factors protecting neurons in prion diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 92%

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Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat　Brain

Motoyoshi-Yamashiro

Takano

Kawabe

et al. 2014

The Journal of Veterinary Medical Science

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“…There is a difference in the obtained results with regards to NO· production degree after the use of iNOS stimulators (lipopolysaccharides and proinflammatory cytokines) in the cultures of microglia, oligodendrocytes, and astrocytes of human origin. While macrophages showed an exceptional expression of iNOS after the stimulation with lipopolysaccharides (Hua et al, 2012), astrocytes produced NO· excessively only as a response to proinflammatory cytokines (Argaw et al, 2012;Motoyoshi-Yamashiro et al, 2013). The obtained differences were interpreted by different effects of the used inducers iNOS on the gene expression of some of the key transcriptional factors, such as nuclear factor-κB (NF-κB), for example, which were expressed in different ways in the tested cell cultures.…”

Section: No· Production and Its Role In Response To Neuroinflammationmentioning

confidence: 99%

Neuroinflammation and demyelination from the point of nitrosative stress as a new target for neuroprotection

Ljubisavljević¹,

Stojanović²

2015

Reviews in the Neurosciences

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AbstractThe role of nitrosative stress in the early pathogenesis of neuroinflammation and demyelination is undoubtedly wide. This review summarizes and integrates the results, found in previously performed studies, which have evaluated nitrosative stress participation in neuroinflammation. The largest number of studies indicates that the supply of nitrosative stress inhibitors has led to the opposite clinical effects in experimental studies. Some results claim that attributing the protective role to nitric oxide, outside the total changes of redox oxidative processes and without following the clinical and paraclinical correlates of neuroinflammation, is an overrated role of this mediator. The fact is that the use of nitrosative stress inhibitors would be justified in the earlier phases of neuroinflammation. The ideal choice would be a specific inducible nitric oxide synthase (iNOS) inhibitor, because its use would preserve the physiological features of nitric oxide produced by the effects of constitutive NOS. This review discusses the antinitrosative therapy as a potential mode of therapy that aims to control neuroinflammation in early phases, delaying its later phases, which are accompanied with irreversible neurological disabilities. Some parameters of nitrosative stress might serve as surrogate biomarkers for neuroinflammation intensity and its radiological and clinical correlates.

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Amphotericin B Increases Transglutaminase 2 Expression Associated with Upregulation of Endocytotic Activity in Mouse Microglial Cell Line BV-2

et al. 2017

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Amphotericin B (AmB), a polyene antibiotic, is reported to cause the microglial activation to induce nitric oxide (NO) production and proinflammatory cytokines expression, and change neurotrophic factors expression in cultured microglia (Motoyoshi et al. in Neurochem Int 52:1290-1296, 2008). On the other hand, tissue-type transglutaminase (TG2) is involved in connection to phagocytes with apoptotic cells. Engulfment of neurons by activated microglia is thought to cause neurodegenerative diseases but detail is unclear, and involvement of TG2 in phagocytosis has been reported in our previous study using lipopolysaccharide-stimulated BV-2 cells (Kawabe et al. in Neuroimmunomodulation 22(4):243-249, 2015). In the present study, we examined the changes of TG2 expression, phagocytosis and pinocytosis in BV-2 cells stimulated by AmB. AmB stimulation increased TG2 expression and TG activity. Phagocytosis of dead cells and pinocytosis of fluorescent microbeads were also up-regulated by AmB stimulation in BV-2 cells. Blockade of TG activity by cystamine, an inhibitor of TGs, suppressed AmB-enhanced TG2 expression, TG activity, NO production, phagocytosis and pinocytosis. Excessive NO production from microglia and/or facilitation of phagocytosis might be involved in neuronal death. To control TG activity might make possible to protect neurons and care for CNS diseases.

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Activation of cultured astrocytes by amphotericin B: Stimulation of NO and cytokines production and changes in neurotrophic factors production

Cited by 6 publications

References 50 publications

Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat　Brain

Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat　Brain

Neuroinflammation and demyelination from the point of nitrosative stress as a new target for neuroprotection

Amphotericin B Increases Transglutaminase 2 Expression Associated with Upregulation of Endocytotic Activity in Mouse Microglial Cell Line BV-2

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Activation of cultured astrocytes by amphotericin B: Stimulation of NO and cytokines production and changes in neurotrophic factors production

Cited by 6 publications

References 50 publications

Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat Brain

Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat Brain

Neuroinflammation and demyelination from the point of nitrosative stress as a new target for neuroprotection

Amphotericin B Increases Transglutaminase 2 Expression Associated with Upregulation of Endocytotic Activity in Mouse Microglial Cell Line BV-2

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Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat　Brain

Amphotericin B Induces Glial Cell Line-Derived Neurotrophic Factor in the Rat　Brain