Effect of progesterone on apoptosis of murine MC3T3-E1 osteoblastic cells |
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Authors: | Qing-Ping Wang Hui Xie Ling-Qing Yuan Xiang-Hang Luo Hui Li Dan Wang Ping Meng Er-Yuan Liao |
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Institution: | (1) Department of Clinical Laboratory, The Third Affiliated Hospital, Suzhou University, 213003 Changzhou, Jiangsu, China;(2) Department of Pediatrics, The Third Affiliated Hospital, Suzhou University, 213003 Changzhou, Jiangsu, China;(3) Institute of Endocrinology and Metabolism, The Second XiangYa Hospital of Central South University, 410011 Changsha, Hunan, China; |
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Abstract: | Progesterone (P) has been suggested as a bone-trophic hormone. Previous studies have shown that P promoted bone formation
by stimulating the proliferation and differentiation of osteoblasts. But, the effect of P on apoptosis of osteoblast in vitro
has not been reported. We propose that P may promote bone formation by suppressing the apoptosis of osteoblast. The present
study was performed to investigate the effect of P on apoptosis of murine MC3T3-E1 osteoblastic cells. Cell apoptosis was
measured by acidine orange/ethidium bromide (AO/EB) staining and sandwich-enzyme-immunoassay. Progesterone receptor (PR),
cytochrome c, caspase-9 and caspase-3 protein levels were determined by Western blot analysis. The enzyme substrate was also used to assess
the activation of caspase-3 and caspase-9. Progesterone suppressed MC3T3-E1 cells apoptosis induced by serum deprivation,
and this effect was blocked by a PR antagonist RU486. Furthermore, the suppressive effects of P on cytochrome c release and caspase-9 and caspase-3 activation in serum-deprived MC3T3-E1 cells were also reversed by RU486. Our study demonstrated
that P protects osteoblast against apoptosis through PR and the downstream mitochondrial pathway. Thus, the data suggest that
the effects of P on osteoblast apoptosis may contribute to the mechanisms by which P exerts its action on bone formation. |
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