Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti‐inflammatory action
Identifieur interne : 000A18 ( Main/Exploration ); précédent : 000A17; suivant : 000A19Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti‐inflammatory action
Auteurs : You-Joung Kim [Corée du Sud] ; Hyun-Jung Park [Corée du Sud] ; Gwang Lee [Corée du Sud] ; Oh Young Bang [Corée du Sud] ; Young Hwan Ahn [Corée du Sud] ; Eunhye Joe [Corée du Sud] ; Hyun Ok Kim [Corée du Sud] ; Phil Hyu Lee [Corée du Sud]Source :
- Glia [ 0894-1491 ] ; 2009-01-01.
English descriptors
Abstract
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)‐α, inducible nitric oxide synthase (iNOS) mRNA expression, and production of NO and TNF‐α 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‐α and iNOS mRNA expression and production of TNF‐α. 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. © 2008 Wiley‐Liss, Inc.
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DOI: 10.1002/glia.20731
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scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>anti‐inflammatory</term><term>mesenchymal stem cells</term><term>neuroprotective effect</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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)‐α, inducible nitric oxide synthase (iNOS) mRNA expression, and production of NO and TNF‐α 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‐α and iNOS mRNA expression and production of TNF‐α. 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. © 2008 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country><settlement><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Kim, You Oung" sort="Kim, You Oung" uniqKey="Kim Y" first="You-Joung" last="Kim">You-Joung Kim</name></noRegion><name sortKey="Ahn, Young Hwan" sort="Ahn, Young Hwan" uniqKey="Ahn Y" first="Young Hwan" last="Ahn">Young Hwan Ahn</name><name sortKey="Bang, Oh Young" sort="Bang, Oh Young" uniqKey="Bang O" first="Oh Young" last="Bang">Oh Young Bang</name><name sortKey="Joe, Eunhye" sort="Joe, Eunhye" uniqKey="Joe E" first="Eunhye" last="Joe">Eunhye Joe</name><name sortKey="Kim, Hyun Ok" sort="Kim, Hyun Ok" uniqKey="Kim H" first="Hyun Ok" last="Kim">Hyun Ok Kim</name><name sortKey="Lee, Gwang" sort="Lee, Gwang" uniqKey="Lee G" first="Gwang" last="Lee">Gwang Lee</name><name sortKey="Lee, Phil Hyu" sort="Lee, Phil Hyu" uniqKey="Lee P" first="Phil Hyu" last="Lee">Phil Hyu Lee</name><name sortKey="Park, Hyun Ung" sort="Park, Hyun Ung" uniqKey="Park H" first="Hyun-Jung" last="Park">Hyun-Jung Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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