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Article

TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production

  • Authors:
    • Fenxi Zhang
    • Tongming Ren
    • Junfang Wu
  • View Affiliations / Copyright

    Affiliations: Department of Anatomy, Sanquan College, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China, Morphology Laboratory, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China
  • Pages: 1224-1228
    |
    Published online on: June 23, 2015
       https://doi.org/10.3892/etm.2015.2590
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Abstract

Bone marrow-derived mesenchymal stem cells (BMSCs) are the most promising seed cells in regenerative medicine. Our previous study demonstrated that transforming growth factor (TGF)-β1 induced BMSC senescence in vitro. Whether TGF‑β1 affects the apoptosis of BMSCs has not been examined; therefore the aim of the present study was to investigate this effect. BMSCs were isolated from mouse bone marrow, and the third‑passage cells were exposed to 0, 10 and 20 ng/ml TGF‑β1 for 24 h. Cell proliferation was measured by MTT assay; apoptosis was assessed using DAPI staining; and the apoptotic signals Annexin V, B‑cell lymphoma (Bcl)‑2 and Bcl‑2‑associated X protein (Bax) were measured using western blotting. Mitochondrial reactive oxygen species (ROS) were measured by flow cytometry following staining with MitoSOX™ Red mitochondrial superoxide indicator. The MTT assay showed that 10 and 20 ng/ml TGF‑β1 inhibited BMSC proliferation. DAPI staining demonstrated that 10 and 20 ng/ml TGF‑β1 promoted BMSC apoptosis, which was further confirmed by a western blotting assay showing a significant increase in the pro‑apoptotic signals Annexin V and Bax but a decrease in the anti‑apoptotic signal Bcl‑2. It was also found that TGF‑β1 markedly increased the mitochondrial ROS levels in BMSCs. It is well known that mitochondrial ROS are strong stimulators of cell apoptosis. These findings indicate that TGF-β1 can induce BMSC apoptosis, and the mechanism may involve mitochondrial ROS generation.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang F, Ren T and Wu J: TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production. Exp Ther Med 10: 1224-1228, 2015.
APA
Zhang, F., Ren, T., & Wu, J. (2015). TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production. Experimental and Therapeutic Medicine, 10, 1224-1228. https://doi.org/10.3892/etm.2015.2590
MLA
Zhang, F., Ren, T., Wu, J."TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production". Experimental and Therapeutic Medicine 10.3 (2015): 1224-1228.
Chicago
Zhang, F., Ren, T., Wu, J."TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production". Experimental and Therapeutic Medicine 10, no. 3 (2015): 1224-1228. https://doi.org/10.3892/etm.2015.2590
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang F, Ren T and Wu J: TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production. Exp Ther Med 10: 1224-1228, 2015.
APA
Zhang, F., Ren, T., & Wu, J. (2015). TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production. Experimental and Therapeutic Medicine, 10, 1224-1228. https://doi.org/10.3892/etm.2015.2590
MLA
Zhang, F., Ren, T., Wu, J."TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production". Experimental and Therapeutic Medicine 10.3 (2015): 1224-1228.
Chicago
Zhang, F., Ren, T., Wu, J."TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production". Experimental and Therapeutic Medicine 10, no. 3 (2015): 1224-1228. https://doi.org/10.3892/etm.2015.2590
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