Open Access
Article
The effect of dexamethasone and hypoxic stress on MC3T3-E1 cells
Zhen-Hong Zhu1,You-Shui Gao1,Bing-Fang Zeng1,Chang-Qing Zhang1
1
Department of Orthopedic Surgery, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University, 600 Yishan Road, Shanghai 200233, China
DOI: 10.2741/3883 Volume 16 Issue 7, pp.2747-2755
Published: 01 June 2011
(This article belongs to the Special Issue Immunoregulation and inflammatory disease)
Abstract

Osteonecrosis of the femoral head (ONFH) can be caused by a decrease in the activity or numbers of osteoblasts, a process in which apoptosis may play an essential role. We investigated the effect of dexamethasone (Dex) combined with hypoxic stress on murine osteoblastic MC3T3-E1 cells. Flow cytometry, western blot and real-time quantitative PCR analyses revealed that hypoxia significantly enhanced Dex-induced apoptosis. Further data demonstrated that both the death receptor and the mitochondria-mediated pathway were involved in Dex-induced apoptosis under hypoxic conditions. However, the death receptor pathway had only a minor effect on this process. The expression levels of Bcl-2 and Bax, which regulate the mitochondria-initiated apoptotic cascade signaling pathway, were significantly different in response to Dex and hypoxia. The mitochondrial membrane potential collapsed, and the inhibitor brain- derived neurotrophic factor (BDNF) conferred effective protection against apoptosis. In summary, the mitochondria-mediated apoptotic pathway functions in osteoblast apoptosis that is induced by Dex in a hypoxic environment, and the present study may help us to gain further insight into the molecular mechanisms of steroid-induced ONFH.

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Zhen-Hong Zhu, You-Shui Gao, Bing-Fang Zeng, Chang-Qing Zhang. The effect of dexamethasone and hypoxic stress on MC3T3-E1 cells. Frontiers in Bioscience-Landmark. 2011. 16(7); 2747-2755.