MicroRNA Profiling of Self-Renewing Human Neural Stem Cells Reveals Novel Sets of Differentially Expressed microRNAs During Neural Differentiation In Vitro

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Publikace nespadá pod Filozofickou fakultu, ale pod Lékařskou fakultu. Oficiální stránka publikace je na webu muni.cz.
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FEDOROVÁ Veronika AMRUZ ČERNÁ Kateřina OPPELT Jan POSPÍŠILOVÁ Veronika BÁRTA Tomáš MRÁZ Marek BOHAČIAKOVÁ Dáša

Rok publikování 2023
Druh Článek v odborném periodiku
Časopis / Zdroj Stem Cell Reviews and Reports
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
www https://link.springer.com/article/10.1007/s12015-023-10524-2
Doi http://dx.doi.org/10.1007/s12015-023-10524-2
Klíčová slova Neural stem cells; microRNA; miRNA sequencing; Cell cycle; Human pluripotent stem cells
Přiložené soubory
Popis The involvement of microRNAs (miRNAs) in orchestrating self-renewal and differentiation of stem cells has been revealed in a number of recent studies. And while in human pluripotent stem cells, miRNAs have been directly linked to the core pluripotency network, including the cell cycle regulation and the maintenance of the self-renewing capacity, their role in the onset of differentiation in other contexts, such as determination of neural cell fate, remains poorly described. To bridge this gap, we used three model cell types to study miRNA expression patterns: human embryonic stem cells (hESCs), hESCs-derived self-renewing neural stem cells (NSCs), and differentiating NSCs. The comprehensive miRNA profiling presented here reveals novel sets of miRNAs differentially expressed during human neural cell fate determination in vitro. Furthermore, we report a miRNA expression profile of self-renewing human NSCs, which has been lacking to this date. Our data also indicates that miRNA clusters enriched in NSCs share the target-determining seed sequence with cell cycle regulatory miRNAs expressed in pluripotent hESCs. Lastly, our mechanistic experiments confirmed that cluster miR-17-92, one of the NSCs-enriched clusters, is directly transcriptionally regulated by transcription factor c-MYC.
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