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Altered expression of apoptosis-related genes in osteocytes exposed to high-dose steroid hormones and hypoxic stress. | LitMetric

AI Article Synopsis

  • High-dose steroid hormones can lead to necrosis of the femoral head, possibly through ischemic hypoxia causing apoptosis in osteocytes.
  • A study used mouse cell lines to analyze gene expression in osteocytes under hypoxic conditions with and without steroid hormone exposure.
  • Results showed that osteocytes exposed to high-dose steroids exhibit increased sensitivity to apoptosis in low-oxygen environments, which may help explain the causes of idiopathic bone necrosis.

Article Abstract

Objective: High-dose steroid hormones cause necrosis of the femoral head. Since steroid hormones function as blood coagulants, we hypothesized that ischemic hypoxia induced by steroid hormones is critical for apoptosis which occurs before necrosis of osteocytes.

Methods: We performed an analysis of gene expression in the process of leading osteocytes to apoptosis, using a mouse cell line. Cultured osteocytes were loaded with hypoxic stress with or without exposure to steroid hormones, and the gene expression under these conditions was investigated using a cDNA array and real-time quantitative RT-PCR.

Results: The proapoptotic p53 gene was downregulated under a hypoxic (1% O2) condition without exposure to steroid hormones. On the other hand, the expression of antiapoptotic Bcl-2 gene was increased by exposure to high-dose steroid hormones under a normoxic condition (20% O2). Interestingly, both proapoptotic (p53 and Bax) and antiapoptotic (Bcl-2 and MDM2)genes were downregulated in osteocytes treated with high-dose steroid hormones in the hypoxic environment.

Conclusions: These findings suggest that osteocytes exposed to high-dose steroid hormones appear to be more sensitive to apoptosis in the hypoxic environment than those without exposure to steroid hormones. This concept helps to understand the pathogenesis of idiopathic necrosis of the bone.

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Source
http://dx.doi.org/10.1159/000099125DOI Listing

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