Journal
MOLECULAR MEDICINE REPORTS
Volume 16, Issue 2, Pages 1685-1690Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2017.6832
Keywords
mesenchymal stem cells; aging; glucose; phosphatidylinositol 3-kinase/Akt and mammalian target of rapamycin signaling
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Funding
- Zhejiang Provincial Foundation of National Science [LY17H250001, LY13H160030]
- Scientific and Technological Developing Scheme of Hangzhou [20130633B33, 20130633B34]
- Science Research Foundation of Zhejiang Health Bureau [2013KYA151, 2016KYB024]
- Traditional Chinese Medicine Science and Technology Project of Zhejiang Province [2016ZA024]
- National College Students Innovation and Entrepreneurship Training Program of China [201513021011]
- Zhejiang Provincial College Students' Science and Technology Innovation Project [2015R401190]
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It has previously been demonstrated that glucose is important in the process of stem cell aging. However, the mechanisms of cell senescence induced by high glucose (HG) remain to be elucidated. The preliminary study indicated that D-galactose induced mesenchymal stem cell (MSCs) aging. The present study demonstrated, following treatment with 11.0 or 22.0 mM HG for 14 days, that HG significantly promoted MSCs aging and the expression levels of phosphorylated (p-) phosphatidylinositol 3-kinase/protein kinase B (Akt) and p-mammalian target of rapamycin signaling (mTOR) in the HG groups were increased compared with the control group. However, following Akt inhibition with 1.0 or 10.0 nM MK-2206, which is an Akt-specific small molecule inhibitor, the senescence-cell value in the HG group was significantly decreased compared with the control group. These results indicated that HG induced MSCs senescence and this effect was primarily mediated via the Akt/mTOR signaling pathway.
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