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miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway

Neural stem/progenitor cells (NSPCs) are self-renewing, multipotent cells and remain in the human brain throughout an individual's lifetime. NSPCs are activated by brain damage and contribute towards repair and motor function recovery in the central nervous system (CNS). It was previously repor...

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Autores principales: Gao, Yunan, Qiao, Hu, Lu, Zhen, Hou, Yuxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691275/
https://www.ncbi.nlm.nih.gov/pubmed/31257508
http://dx.doi.org/10.3892/mmr.2019.10445
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author Gao, Yunan
Qiao, Hu
Lu, Zhen
Hou, Yuxia
author_facet Gao, Yunan
Qiao, Hu
Lu, Zhen
Hou, Yuxia
author_sort Gao, Yunan
collection PubMed
description Neural stem/progenitor cells (NSPCs) are self-renewing, multipotent cells and remain in the human brain throughout an individual's lifetime. NSPCs are activated by brain damage and contribute towards repair and motor function recovery in the central nervous system (CNS). It was previously reported that miR-29 was involved in regulating proliferation, differentiation and survival in hepatocellular carcinoma, and osteoblast and mantle cell lymphoma; however, the effects of miR-29 on NSPCs remain unclear. In the present study, it was demonstrated via Cell Counting Kit-8 assays that overexpression of miR-29 promoted the viability of NPSCs, and downregulated the expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) protein. Additionally, treatment with a PTEN-specific inhibitor (VO-OHpic trihydrate) abolished the effects of the miR-29 inhibitor on PTEN expression, as determined via western blotting. Flow cytometry and 5-bromo-2-deoxyuridine (BrdU) staining revealed that overexpression of miR-29 further promoted the proliferation of NSPCs; however, knocking down miR-29 inhibited cell proliferation. VO-OHpic trihydrate reversed the effects of miR-29 knockdown on cell proliferation. Furthermore, it was observed that overexpression of miR-29 increased the phosphorylation levels of AKT. Collectively, the results indicated that overexpression of miR-29 promoted the proliferation of cultured rat NSPCs and decreased the expression of PTEN protein, and that the activation of Akt may be a potential underlying mechanism. The present findings may provide novel insight for the development of strategies for stem cell-mediated treatment of CNS diseases.
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spelling pubmed-66912752019-08-19 miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway Gao, Yunan Qiao, Hu Lu, Zhen Hou, Yuxia Mol Med Rep Articles Neural stem/progenitor cells (NSPCs) are self-renewing, multipotent cells and remain in the human brain throughout an individual's lifetime. NSPCs are activated by brain damage and contribute towards repair and motor function recovery in the central nervous system (CNS). It was previously reported that miR-29 was involved in regulating proliferation, differentiation and survival in hepatocellular carcinoma, and osteoblast and mantle cell lymphoma; however, the effects of miR-29 on NSPCs remain unclear. In the present study, it was demonstrated via Cell Counting Kit-8 assays that overexpression of miR-29 promoted the viability of NPSCs, and downregulated the expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) protein. Additionally, treatment with a PTEN-specific inhibitor (VO-OHpic trihydrate) abolished the effects of the miR-29 inhibitor on PTEN expression, as determined via western blotting. Flow cytometry and 5-bromo-2-deoxyuridine (BrdU) staining revealed that overexpression of miR-29 further promoted the proliferation of NSPCs; however, knocking down miR-29 inhibited cell proliferation. VO-OHpic trihydrate reversed the effects of miR-29 knockdown on cell proliferation. Furthermore, it was observed that overexpression of miR-29 increased the phosphorylation levels of AKT. Collectively, the results indicated that overexpression of miR-29 promoted the proliferation of cultured rat NSPCs and decreased the expression of PTEN protein, and that the activation of Akt may be a potential underlying mechanism. The present findings may provide novel insight for the development of strategies for stem cell-mediated treatment of CNS diseases. D.A. Spandidos 2019-09 2019-07-01 /pmc/articles/PMC6691275/ /pubmed/31257508 http://dx.doi.org/10.3892/mmr.2019.10445 Text en Copyright: © Gao et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Gao, Yunan
Qiao, Hu
Lu, Zhen
Hou, Yuxia
miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway
title miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway
title_full miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway
title_fullStr miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway
title_full_unstemmed miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway
title_short miR-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway
title_sort mir-29 promotes the proliferation of cultured rat neural stem/progenitor cells via the pten/akt signaling pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691275/
https://www.ncbi.nlm.nih.gov/pubmed/31257508
http://dx.doi.org/10.3892/mmr.2019.10445
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