| Registro completo |
| Provedor de dados: |
Biol. Res.
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| País: |
Chile
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| Título: |
Suppression of miR-181 a attenuates H2O2-induced death of mesenchymal stem cells by maintaining hexokinase II expression
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| Autores: |
Lee,Seahyoung
Yun,Ina
Ham,Onju
Lee,Se-Yeon
Lee,Chang Yeon
Park,Jun-Hee
Lee,Jiyun
Seo,Hyang-Hee
Choi,Eunhyun
Hwang,Ki-Chul
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| Data: |
2015-01-01
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| Ano: |
2015
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| Palavras-chave: |
Hexokinase II
MiRNA-181a
Cell death
Mesenchymal stem cell
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| Resumo: |
BACKGROUND: Low survival rate of transplanted cells compromises the efficacy of cell therapy. Hexokinase II (HKII) is known to have anti-apoptotic activity through its interaction with mitochondria. The objective was to identify miRNAs targeting HKII and investigate whether miRNA-mediated modulation of HKII could improve the survival of mesenchymal stem cells (MSCs) exposed to H2O2. The expression of HKII in MSCs exposed to H2O2 was evaluated, and HKII-targeting miRNA was screened based on miRNA-target prediction databases. The effect of H2O2 on the expression of the selected HKII-targeting miRNA was examined and the effect of modulation of the selected HKII-targeting miRNA using anti-miRNA on H2O2-induced apoptosis of MSC was evaluated. RESULTS: H2O2 (600 μΜ) induced cell death of MSCs and decreased mitochondrial HKII expression. We have identified miR-181a as a HKII-targeting miRNA and H2O2 increased the expression of miR-181a in MSCs. Delivery of anti-miR-181a, which neutralizes endogenous miR-181a, significantly attenuated H2O2-induced decrease of HKII expression and disruption of mitochondrial membrane potential, improving the survival of MSCs exposed to H2O2. CONCLUSIONS: These findings suggest that H2O2-induced up-regulation of miR-181a contributes to the cell death of MSCs by down-regulating HKII. Neutralizing miR-181a can be an effective way to prime MSCs for transplantation into ischemic tissues.
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| Tipo: |
Journal article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602015000100045
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| Editor: |
Sociedad de Biología de Chile
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| Formato: |
text/html
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| Fonte: |
Biological Research v.48 2015
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