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Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis

  • Authors:
    • Jiang Rui
    • Shaohong Fang
    • Yongchen Wang
    • Bo Lv
    • Bo Yu
    • Shufeng Li
  • View Affiliations / Copyright

    Affiliations: General Practice Department, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China, Key Laboratory of the Education Ministry for Myocardial Ischemia Mechanism and Treatment, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China
    Copyright: © Rui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 902-910
    |
    Published online on: May 11, 2018
       https://doi.org/10.3892/mmr.2018.9012
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Abstract

Bone marrow‑derived mesenchymal stem cells (BM‑MSCs) have been used in experimental research and clinical trials for heart function restoration and cardiomyocyte regeneration. However, due to a hostile microenvironment created by ischemia, hypoxia and pro‑inflammatory factors, the survival rate of implanted BM‑MSCs remains low. Therefore, strategies that can promote BM‑MSC survival and prevent apoptosis are required. Previous studies have reported that microRNA‑16 (miR‑16) can inhibit cell proliferation by targeting several proteins and signal pathway, not only by inducing apoptosis. In the present study, it was investigated whether inhibition of miR‑16 reduced BM‑MSC apoptosis in a model of ischemia. Flow cytometry analysis revealed that BM‑MSCs underwent apoptosis in response to hypoxia/serum deprivation (SD). Additionally, in hypoxic/SD conditions, miR‑16 expression increased and B‑cell lymphoma (Bcl)‑2 protein expression decreased in BM‑MSCs. miR‑16 did not affect Bcl‑2 mRNA expression but downregulated Bcl‑2 protein expression. miR‑16 inhibitor transfection significantly increased Bcl‑2 protein expression and the percentage of apoptotic BM‑MSCs was reduced. The pro‑apoptotic effects of miR‑16 were partially elevated by knocking down of Bcl‑2. Furthermore, it was demonstrated that miR‑16 exerted its pro‑apoptotic effects by activating the mitochondrial pathway of apoptosis via apoptotic protease activating factor‑1/caspase‑9/poly (ADP ribose) polymerase. Taken together, the results indicated that miR‑16 downregulated Bcl‑2 expression and promoted BM‑MSC apoptosis, indicating that therapies targeting miR‑16 may improve the effectiveness of BM‑MSC transplantation therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Rui J, Fang S, Wang Y, Lv B, Yu B and Li S: Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis. Mol Med Rep 18: 902-910, 2018.
APA
Rui, J., Fang, S., Wang, Y., Lv, B., Yu, B., & Li, S. (2018). Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis. Molecular Medicine Reports, 18, 902-910. https://doi.org/10.3892/mmr.2018.9012
MLA
Rui, J., Fang, S., Wang, Y., Lv, B., Yu, B., Li, S."Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis". Molecular Medicine Reports 18.1 (2018): 902-910.
Chicago
Rui, J., Fang, S., Wang, Y., Lv, B., Yu, B., Li, S."Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis". Molecular Medicine Reports 18, no. 1 (2018): 902-910. https://doi.org/10.3892/mmr.2018.9012
Copy and paste a formatted citation
x
Spandidos Publications style
Rui J, Fang S, Wang Y, Lv B, Yu B and Li S: Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis. Mol Med Rep 18: 902-910, 2018.
APA
Rui, J., Fang, S., Wang, Y., Lv, B., Yu, B., & Li, S. (2018). Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis. Molecular Medicine Reports, 18, 902-910. https://doi.org/10.3892/mmr.2018.9012
MLA
Rui, J., Fang, S., Wang, Y., Lv, B., Yu, B., Li, S."Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis". Molecular Medicine Reports 18.1 (2018): 902-910.
Chicago
Rui, J., Fang, S., Wang, Y., Lv, B., Yu, B., Li, S."Inhibition of microRNA‑16 protects mesenchymal stem cells against apoptosis". Molecular Medicine Reports 18, no. 1 (2018): 902-910. https://doi.org/10.3892/mmr.2018.9012
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