Glucocorticoids induce apoptosis by inhibiting microRNA cluster miR‑17‑92 expression in chondrocytic cells
Wenhua Xing1, Lixia Hao2, Xuejun Yang1
1Department of Spinal Surgery, Second Affiliated Hospital of Inner Mongolia Medical University, Huimin, Hohhot, Inner Mongolia Autonomous Region 010058, P.R. China.
Abstract:
Sustained treatment with glucocorticoids (GCs) has frequently been observed to impair skeletal development. However, the influence of GCs on chondrocytes, which have a key role in skeletal development, has been rarely reported. HCS‑2/8 cells were selected as an in vitro model of human chondrocytes to assess the apoptosis induced by GCs and determine the role of the microRNA‑17‑92 (miR‑17‑92) cluster in the regulation of apoptosis. It was demonstrated that dexamethasone (Dex) was able to induce apoptosis and high levels of expression of apoptosis‑associated molecules in HCS‑2/8 chondrocytic cells, and that expression of the miR‑17‑92 cluster was inhibited during Dex‑induced apoptosis. In conclusion, the present study suggested that inhibition of the expression of the miR‑17‑92 cluster contributed to the Dex‑induced apoptosis in chondrocytes. The results suggest that microRNAs have an important role in glucocorticoid‑induced impairment to chondrocytes.
Insights
Glucocorticoids (GCs) induce chondrocyte apoptosis by inhibiting the microRNA-17-92 (miR-17-92) cluster. This suggests microRNAs play a key role in GC-induced skeletal development impairment.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- Sustained glucocorticoid (GC) treatment impairs skeletal development.
- The specific effects of GCs on chondrocytes, crucial for skeletal development, are under-investigated.
- Understanding GC-induced chondrocyte apoptosis is vital for skeletal health.
Purpose of the Study:
- To investigate the role of the microRNA-17-92 (miR-17-92) cluster in GC-induced chondrocyte apoptosis.
- To utilize HCS-2/8 cells as an in vitro model for human chondrocytes.
- To elucidate the molecular mechanisms underlying GC effects on chondrocytes.
Main Methods:
- Utilized HCS-2/8 cells as an in vitro model of human chondrocytes.
- Administered dexamethasone (Dex) to induce apoptosis.
- Assessed apoptosis-associated molecule expression.
- Measured the expression levels of the miR-17-92 cluster.
Main Results:
- Dexamethasone (Dex) induced apoptosis in HCS-2/8 chondrocytic cells.
- Dex treatment led to high expression of apoptosis-associated molecules.
- Expression of the miR-17-92 cluster was significantly inhibited during Dex-induced apoptosis.
Conclusions:
- Inhibition of the miR-17-92 cluster contributes to Dex-induced apoptosis in chondrocytes.
- MicroRNAs are implicated in glucocorticoid-induced impairment of chondrocytes.
- The miR-17-92 cluster may serve as a potential therapeutic target for mitigating GC-induced skeletal damage.
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