Glucocorticoids induce autophagy in rat bone marrow mesenchymal stem cells

Glucocorticoid-induced osteoporosis (GIOP) is a widespread clinical complication following glucocorticoid therapy. This irreversible damage to bone-forming and -resorbing cells is essential in the pathogenesis of osteoporosis. Autophagy is a physiological process involved in the regulation of cells...

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Published inMolecular medicine reports Vol. 11; no. 4; pp. 2711 - 2716
Main Authors WANG, LONG, FAN, JING, LIN, YAN-SHUI, GUO, YUN-SHAN, GAO, BO, SHI, QI-YUE, WEI, BO-YUAN, CHEN, LI, YANG, LIU, LIU, JIAN, LUO, ZHUO-JING
Format Journal Article
LanguageEnglish
Published Greece D.A. Spandidos 01.04.2015
Spandidos Publications
Spandidos Publications UK Ltd
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Summary:Glucocorticoid-induced osteoporosis (GIOP) is a widespread clinical complication following glucocorticoid therapy. This irreversible damage to bone-forming and -resorbing cells is essential in the pathogenesis of osteoporosis. Autophagy is a physiological process involved in the regulation of cells and their responses to diverse stimuli, however, the role of autophagy in glucocorticoid-induced damage to bone marrow mesenchymal stem cells (BMSCs) remains unclear. The current study confirmed that glucocorticoid administration impaired the proliferation of BMSCs. Transmission electron microscopy, immunohistochemistry and western blot analysis detected autophagy in vitro and in GIOP model rats (in vivo). With the addition of the autophagy inhibitor 3-methyladenine, the proliferative ability of BMSCs was further reduced, while the number of apoptotic BMSCs was significantly increased. The data suggests that in response to glucocorticoid administration, induced autophagy aids to maintain proliferation and prevent apoptosis of BMSCs. Thus, it is hypothesized that autophagy may be a novel target in the treatment or prevention of osteoporosis.
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ISSN:1791-2997
1791-3004
DOI:10.3892/mmr.2014.3099