Repetitive magnetic stimulation promotes neural stem cells proliferation by upregulating MiR-106b in vitro / 华中科技大学学报(医学)(英德文版)
J. huazhong univ. sci. tech. med. sci
; (6): 766-772, 2015.
Article
de En
| WPRIM
| ID: wpr-250343
Bibliothèque responsable:
WPRO
ABSTRACT
Neural stem cells (NSCs) proliferation can be influenced by repetitive transcranial magnetic stimulation (rTMS) in vivo via microRNA-106b-25 cluster, but the underlying mechanisms are poorly understood. This study investigated the involvement of microRNA-106b-25 cluster in the proliferation of NSCs after repetitive magnetic stimulation (rMS) in vitro. NSCs were stimulated by rMS (200/400/600/800/1000 pulses per day, with 10 Hz frequency and 50% maximum machine output) over a 3-day period. NSCs proliferation was detected by using ki-67 and EdU staining. Ki-67, p21, p57, cyclinD1, cyclinE, cyclinA, cdk2, cdk4 proteins and miR-106b, miR-93, miR-25 mRNAs were detected by Western blotting and qRT-PCR, respectively. The results showed that rMS could promote NSCs proliferation in a dose-dependent manner. The proportions of ki-67+ and Edu+ cells in 1000 pulses group were 20.65% and 4.00%, respectively, significantly higher than those in control group (9.25%, 2.05%). The expression levels of miR-106b and miR-93 were significantly upregulated in 600-1000 pulses groups compared with control group (P<0.05 or 0.01 for all). The expression levels of p21 protein were decreased significantly in 800/1000 pulses groups, and those of cyclinD1, cyclinA, cyclinE, cdk2 and cdk4 were obviously increased after rMS as compared with control group (P<0.05 or 0.01 for all). In conclusion, our findings suggested that rMS enhances the NSCs proliferation in vitro in a dose-dependent manner and miR-106b/p21/cdks/cyclins pathway was involved in the process.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Marqueurs biologiques
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Transduction du signal
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Régulation de l'expression des gènes
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Rat Sprague-Dawley
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Cyclines
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Antigène KI-67
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Biologie cellulaire
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MicroARN
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Prolifération cellulaire
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Kinase-2 cycline-dépendante
Limites du sujet:
Animals
langue:
En
Texte intégral:
J. huazhong univ. sci. tech. med. sci
Année:
2015
Type:
Article