Dataset Information

MiR-21 increases c-kit⁺ cardiac stem cell proliferation in vitro through PTEN/PI3K/Akt signaling.

ABSTRACT: The low survival rate of cardiac stem cells (CSCs) in the ischemic myocardium is one of the obstacles in ischemic cardiomyopathy cell therapy. The MicroRNA (miR)-21 and one of its target protein, the tensin homolog deleted on chromosome ten (PTEN), contributes to the proliferation of many kinds of tissues and cell types. It is reported that miR-21 promotes proliferation through PTEN/PI3K/Akt pathway, but its effects on c-kit⁺ CSC remain unclear. The authors hypothesized that miR-21 promotes the proliferation in c-kit ⁺ CSC, and evaluated the involvement of PTEN/PI3K/Akt pathway in vitro. miR-21 up-regulation with miR-21 efficiently mimics accelerated cell viability and proliferation in c-kit ⁺ CSC, which was evidenced by the CCK-8, EdU and cell cycle analyses. In addition, the over-expression of miR-21 in c-kit ⁺ CSCs notably down-regulated the protein expression of PTEN although the mRNA level of PTEN showed little change. Gain-of-function of miR-21 also increased the phosphor-Akt (p-Akt) level. Phen, the selective inhibitor of PTEN, reproduced the pro-proliferation effects of miR-21, while PI3K inhibitor, LY294002, totally attenuated the pro-survival effect of miR-21. These results indicate that miR-21 is efficient in promoting proliferation in c-kit⁺ CSCs, which is contributed by the PTEN/PI3K/Akt pathway. miR-21 holds the potential to facilitate CSC therapy in ischemic myocardium.

SUBMITTER: Shi B

PROVIDER: S-EPMC5289448 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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miR-21 increases c-kit+ cardiac stem cell proliferation in vitro through PTEN/PI3K/Akt signaling.

Shi Bei B Deng Wenwen W Long Xianping X Zhao Ranzun R Wang Yan Y Chen Wenming W Xu Guanxue G Sheng Jin J Wang Dongmei D Cao Song S

PeerJ 20170105

The low survival rate of cardiac stem cells (CSCs) in the ischemic myocardium is one of the obstacles in ischemic cardiomyopathy cell therapy. The MicroRNA (miR)-21 and one of its target protein, the tensin homolog deleted on chromosome ten (PTEN), contributes to the proliferation of many kinds of tissues and cell types. It is reported that miR-21 promotes proliferation through PTEN/PI3K/Akt pathway, but its effects on c-kit+ CSC remain unclear. The authors hypothesized that miR-21 pr ...[more]

PMID: 28168101

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Project description:The present study aimed to investigate the effects of microRNA (miR)?21 on osteoclastogenesis and its underlying molecular mechanisms. The expression levels of tartrate?resistant acid phosphatase (TRAP) and miR?21 were detected during osteoclastogenesis in receptor activator of NF??B ligand (RANKL)?induced RAW264.7 cells via reverse transcription?quantitative PCR. Bioinformatics and dual luciferase reporter assays were performed to analyze the association between miR?21 and Pten. RANKL?induced RAW264.7 cells were divided into the following groups: MiR?negative control (NC), miR?21 mimic, miR?21 inhibitor and miR?21 mimic + LY294002. The effects of miR?21 on osteoclastogenesis and bone resorption were then detected using TRAP staining and a bone resorption assay. Pten, phosphorylated?Akt and nuclear factor of activated T cell (NFATc1) expression levels were measured by western blotting to analyze the effects of miR?21 on the PI3K/Akt signaling pathway. The present study revealed that miR?21 was upregulated during osteoclastogenesis in RANKL?induced RAW264.7 cells. Furthermore, miR?21 negatively regulated Pten. Compared with the miR?negative control (NC) group, the number of osteoclasts and the percentage of bone resorption were increased in the miR?21 mimic group, whereas they were decreased in the miR?21 inhibitor group. The number of osteoclasts and the percentage of bone resorption in the miR?21 mimic + LY294002 group were lower than in the miR?21 mimic group. Compared with the miR?NC group, the protein expression levels of Pten were decreased, whereas p?Akt and NFATc1 were increased in the miR?21 mimic group. Conversely, Pten protein expression was increased, whereas p?Akt and NFATc1 were decreased in the miR?21 inhibitor group. In the miR?21 mimic + LY294002 group, Pten protein expression was higher, and p?Akt and NFATc1 were lower than in the miR?21 mimic group. In conclusion, miR?21 is upregulated during osteoclastogenesis, and may promote osteoclastogenesis and bone resorption through activating the PI3K/Akt signaling pathway via targeting Pten.

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MiR-21 increases c-kit⁺ cardiac stem cell proliferation in vitro through PTEN/PI3K/Akt signaling.

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miR-21 increases c-kit<sup>+</sup> cardiac stem cell proliferation <i>in vitro</i> through PTEN/PI3K/Akt signaling.

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MiR-21 increases c-kit+ cardiac stem cell proliferation in vitro through PTEN/PI3K/Akt signaling.

Publications

miR-21 increases c-kit<sup>+</sup> cardiac stem cell proliferation <i>in vitro</i> through PTEN/PI3K/Akt signaling.

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OmicsDI is part of the ELIXIR infrastructure

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MiR-21 increases c-kit⁺ cardiac stem cell proliferation in vitro through PTEN/PI3K/Akt signaling.