NDLI: Effect of progesterone on apoptosis of murine MC3T3-E1 osteoblastic cells

Content Provider	Springer Nature Link
Author	Wang, Qing Ping Xie, Hui Yuan, Ling Qing Luo, Xiang Hang Li, Hui Wang, Dan Meng, Ping Liao, Er Yuan
Copyright Year	2008
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.
Starting Page	57
Ending Page	63
Page Count	7
File Format	PDF
ISSN	09394451
Journal	Amino Acids
Volume Number	36
Issue Number	1
e-ISSN	14382199
Language	English
Publisher	Springer Vienna
Publisher Date	2008-02-06
Publisher Place	Vienna
Access Restriction	Subscribed
Subject Keyword	Progesterone Apoptosis Osteoblast Neurobiology Proteomics Life Sciences Biochemical Engineering Analytical Chemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Organic Chemistry Biochemistry Clinical Biochemistry

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