Vanadate inhibits dexamethasone-induced apoptosis of rat bone marrow-derived mesenchymal stem cells

Ann Clin Lab Sci. 2015 Spring;45(2):173-80.

Abstract

Apoptosis of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been shown to contribute to the development of osteoporosis, which is often the result of long-term use of glucocorticoid drugs such as dexamethasone (Dex). However, it remains unknown whether Dex induces apoptosis of BM-MSCs, and whether a chemical agent like vanadate can block such effects. To investigate these two issues, we isolated BM-MSCs from SD rats and treated the cells with different doses of Dex. We found that Dex induced apoptosis in dose- and time-dependent manners. Pretreating BM-MSCs with vanadate prevented Dex-induced apoptosis. Furthermore, we found that expression of caspases (3, 8, and 9) increased in Dex-treated BM-MSC and was attenuated by vanadate pretreatment. These results not only demonstrate the role of vanadate in the inhibition of Dex-induced apoptosis of BM-MSCs, but also reveal the therapeutic potential of vanadate in glucocorticoid-mediated osteoporosis.

Keywords: BM-MSCs; apoptosis; caspase; glucocorticoid; vanadate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Bone Marrow Cells / cytology*
  • Caspases / metabolism
  • Cell Proliferation / drug effects
  • Dexamethasone / pharmacology*
  • Mesenchymal Stem Cells / cytology*
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / enzymology
  • Rats
  • Vanadates / pharmacology*

Substances

  • Vanadates
  • Dexamethasone
  • Caspases