Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (11): 1905-1908.doi: 10.3969/j.issn.1673-8225.2011.11.002

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Regulation of estrogen for chondrocyte proliferation in the rib growth plate

Li Ji-bin1, Li Hai-qi2, Wang Song-yan2   

  1. 1Department of Nutrition and Food Hygiene, School of Public Health, Chongqing Medical University, Chongqing  400016, China
    2Department of Children’s Health Care, Children’s Hospital, Chongqing Medical University, Chongqing  400012, China
  • Received:2010-09-01 Revised:2010-12-07 Online:2011-03-12 Published:2011-03-12
  • About author:Li Ji-bin☆, Doctor, Associate professor, Department of Nutrition and Food Hygiene, School of Public Health, Chongqing Medical University, Chongqing 400016, China ljb21st@126.com
  • Supported by:

    the Subject of Healthy Bureau of Chongqing, No. 99-2022*

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Abstract:

BACKGROUND: Estrogen is an indispensable factor in the closure of growth plate. However, no experiment studies the effect of estrogen on chondrocytes proliferation, cell cycle or ultrastructure alteration during apoptosis. 
OBJECTIVE: To explore the effects of estrogen on regulating chondrocytes proliferation and senescence of the ribs growth plate.
METHODS: Totally 30 New Zealand white rabbits were prepared for ovariectomized models and received either estradiol benzoate (estradiol group) or sterilized cottonseed oil (model group). All rabbits were sacrificed at 23, 26 and 29 weeks. BrdU was subcutaneous injected at 7 and 1 hours before execution. The BrdU positive rate of growth plates from the ribs was detected by immunohistochemistry. The chondrocytes cell cycle was examined by flow cytometry, and ultrastructure was observed by a transmission electron microscope.
RESULTS AND CONCLUSION: BrdU positive-staining rate of both groups were gradually decreased. During early time (23 to 26 weeks of age), the percentage of BrdU positive-staining chondrocytes in the estradiol group were higher than those of the model group (P < 0.05), but the differences had no significance at 39 weeks of age (P > 0.05). After the injection of estradiol, there were accumulations of chondrocytes in the S phase of the rib growth plate with higher proliferation index. By the end of the experiment the proliferation index was decreased. Our data suggested that chondrocyte proliferation was enhanced by estrogen during the early time with significant replicative senescence induced thereafter and causing the process of growth plate senescence.

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