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Published on: June 12, 2017
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Glucocorticoids induce autophagy in rat bone marrow mesenchymal stem cells
Long Wang1, Jing Fan1, Yan-Shui Lin2
1Department of Orthopedics, Institute of Orthopedic Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Molecular Medicine Reports
|December 18, 2014
Summary
Glucocorticoid-induced osteoporosis (GIOP) involves damage to bone cells. This study shows that induced autophagy helps maintain bone marrow mesenchymal stem cell (BMSC) proliferation and prevents apoptosis, suggesting autophagy as a potential therapeutic target for GIOP.
Area of Science:
- Biomedical Sciences
- Cell Biology
- Bone Biology
Background:
- Glucocorticoid-induced osteoporosis (GIOP) is a common complication of glucocorticoid therapy.
- The pathogenesis of GIOP involves damage to bone-forming and bone-resorbing cells.
- The specific role of autophagy in glucocorticoid-induced damage to bone marrow mesenchymal stem cells (BMSCs) is not well understood.
Purpose of the Study:
- To investigate the role of autophagy in the response of BMSCs to glucocorticoid administration.
- To determine if autophagy influences BMSC proliferation and apoptosis under glucocorticoid treatment.
Main Methods:
- In vitro and in vivo experiments using GIOP model rats.
- Transmission electron microscopy, immunohistochemistry, and western blot analysis to detect autophagy.
- Administration of the autophagy inhibitor 3-methyladenine to assess its effects on BMSCs.
Main Results:
- Glucocorticoid administration was confirmed to impair BMSC proliferation.
- Autophagy was detected in BMSCs both in vitro and in vivo in GIOP models.
- Inhibition of autophagy led to further reduced BMSC proliferation and increased BMSC apoptosis.
Conclusions:
- Induced autophagy plays a protective role in maintaining BMSC proliferation and preventing apoptosis during glucocorticoid exposure.
- Autophagy is a potential novel therapeutic target for the prevention or treatment of glucocorticoid-induced osteoporosis.
