Regulating Factors for Microglial Activation.

Nakamura, Yoichi

doi:10.1248/bpb.25.945

Cited by 214 publications

(118 citation statements)

References 145 publications

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“…Furthermore, hMSCs decreased production of TNF-a and iNOS from microglia stimulated by LPS in a contact-independent manner. Although the precise mechanism of the inhibitory effect of MSCs on microglial activation is unknown, there is ample evidence that microglial activation can be modulated by various cytokines and neurotrophic factors (Hanisch and Kettenmann, 2007;Nakamura, 2002;Oh et al, 2008). Therefore, it is speculated that soluble factors released from MSCs, such as IL-6, IL-10, and TGF-b may regulate the microglia response to LPS in our experiment.…”

Section: Discussionmentioning

confidence: 84%

Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti‐inflammatory action

Kim

Park

Lee

et al. 2008

Glia

211

170

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Parkinson's disease (PD) is a common, progressive neurodegenerative disorder caused by the loss of dopaminergic neurons in the substantia nigra (SN). Numerous studies have provided evidence suggesting that neuroinflammation plays an important role in the pathogenesis of PD. In this study, we used lipopolysaccharide (LPS)-induced in vitro and in vivo inflammation models to investigate whether human mesenchymal stem cells (hMSCs) have a protective effect on the dopaminergic system through anti-inflammatory mechanisms. The hMSC treatment significantly decreased LPS-induced microglial activation, tumor necrosis factor (TNF)-a, inducible nitric oxide synthase (iNOS) mRNA expression, and production of NO and TNF-a compared with the LPS-only treatment group. In co-cultures of microglia and mesencephalic dopaminergic neurons, hMSC treatment significantly decreased the loss of tyrosine hydroxylase-immunopositive (TH-ip) cells. The hMSC treatment in rats showed that TH-ip neuronal loss induced by LPS stimulation in the SN was considerably decreased and was clearly accompanied by a decrease in activation of microglia, as well as TNF-a and iNOS mRNA expression and production of TNF-a. These data suggest that hMSCs have a neuroprotective effect on dopaminergic neurons through anti-inflammatory actions mediated by the modulation of microglial activation. Along with various trophic effects and trans-differentiational potency, the anti-inflammatory properties of MSCs could have major therapeutic implications in the treatment of PD. V V C

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Section: Discussionmentioning

confidence: 84%

Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti‐inflammatory action

Kim

Park

Lee

et al. 2008

Glia

211

170

View full text Add to dashboard Cite

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“…Although the signals that activate microglia in vivo are defined incompletely, several studies using in vitro models have shown that microglia respond to cytokines (IL-1 , TNF-and IFN-), microbial products, such as bacterial LPS, and certain diseaserelated abnormal proteins, including -amyloid, human immunodeficiency virus (HIV)-specific gp41 and HIV-Tat, prions (Nakamura et al, 2002), and heat shock proteins (Kakimura et al, 2002). These factors activate their receptors and activate intracellular signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of 8-hydroxydeoxyguanosine in LPS-induced microglia activation: suppression of STAT3-mediated intercellular adhesion molecule-1 expression

Kim

Cho²,

Kim³

et al. 2006

Exp Mol Med

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“…Anti-inflammatory compounds have been studied as a therapy for Alzheimer's disease and other degenerative diseases and injuries of brain (McGeer & McGeer, 1995). The microglial activation process itself as well as the factors that stimulate and inhibit the inflammatory response have been intensively studied and reviewed in detail (Nakamura, 2002).…”

Section: Introductionmentioning

confidence: 99%

Regulation of microglial inflammatory response by sodium butyrate and short‐chain fatty acids

Huuskonen

Suuronen

Nuutinen

et al. 2004

British J Pharmacology

215

147

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1 Recent studies have shown that sodium butyrate and other short-chain fatty acids (SCFAs) can prevent inflammation in colon diseases. Our aim was to elucidate whether sodium butyrate and SCFAs regulate the inflammatory responses in different neural inflammation models in cell cultures. 2 Inflammatory responses to LPS-induced microglial activation were recorded by the secretion of nitric oxide (NO) and cytokines IL-6 and TNF-a and related to the changes in the DNA-binding activities of NF-kB complex. 3 We observed that sodium butyrate is strongly anti-inflammatory against LPS-induced responses in rat primary microglia as well as in hippocampal slice cultures and in neural cocultures of microglial cells, astrocytes and cerebellar granule neurons. 4 In murine N9 microglial cell line, instead, sodium butyrate and other SCFAs (propionate, valerate and caproate) enhanced the LPS-induced inflammatory response. 5 The pretreatment with butyrate before LPS exposure induced an equal or more enhanced response than simultaneous exposure with butyrate and LPS. This indicates that butyrate induces an adaptative response against microglial activation. 6 We also observed that butyrate treatment both in transformed N9 cells and in hippocampal slice cultures downregulates the NF-kB-binding capacity induced by LPS stimulation. 7 Our results show that butyrate is anti-inflammatory in primary, brain-derived microglial cells, as observed recently in colon diseases, but proinflammatory in transformed, proliferating N9 microglial cells, which may be related to the anticancer properties of butyrate observed in tumor cells.

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Regulating Factors for Microglial Activation.

Cited by 214 publications

References 145 publications

Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti‐inflammatory action

Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti‐inflammatory action

Anti-inflammatory effects of 8-hydroxydeoxyguanosine in LPS-induced microglia activation: suppression of STAT3-mediated intercellular adhesion molecule-1 expression

Regulation of microglial inflammatory response by sodium butyrate and short‐chain fatty acids

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