Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (32): 5915-5919.doi: 10.3969/j.issn.2095-4344.2012.32.005

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Prolyl hydroxylase inhibitor prevents bone marrow mesenchymal stem cells apoptosis in mice

Zhang Lei, Zhao Xue-ling, Li Biao, Liu Jin-song, Li Xi, Gong Yue-kun   

  1. Department of Orthopedics, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
  • Received:2011-10-11 Revised:2011-12-01 Online:2012-08-05 Published:2012-08-05
  • Contact: Gong Yue-kun, Chief physician, Department of Orthopedics, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China gongyuekun@yahoo.com.cn
  • About author:Zhang Lei☆, Studying for doctorate, Department of Orthopedics, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China lzhang670252@163.com

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Abstract:

BACKGROUND: Prolyl hydroxylase inhibitors can stabilize hypoxia inducible factor to up-regulate downstream genes expression, thereby regulating cell apoptosis.
OBJECTIVE: To evaluate the effects of the prolyl hydroxylase inhibitors dimethyloxalglycine (DMOG) on apoptosis of bone marrow-derived mesenchymal stem cells (BMSCs) induced by serum deprivation.
METHODS: Bone marrow mononuclear cells were harvested from Kunming mice bone marrow cavity of the femur and tibia and subcultured. The passage five mononuclear cells were identified by flow cytometry and tri-lineage differentiation. Bone marrow mononuclear cells were cultured in serum-free DMEM for serum deprivation (serum-deprivation group) and DMEM containing 10% fetal bovine serum (normal control group) for 24, 48, and 72 hours. Experimental group was treated with 1 mmol/L DMOG based on serum-free culture.
RESULTS AND CONCLUSION: The bone marrow mononuclear cells from the mice were purified through subculture and were verified as BMSCs through cell surface marker identification by flow cytometry. Compared with serum-deprivation group, the apoptosis rate was significantly decreased in experimental group (P < 0.01). Results indicate that DMOG can suppress BMSCs apoptosis induced by serum deprivation.

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