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Interactions between glucocorticoids and cytokines in the bone microenvironment.
A Angeli1, A Dovio, M L Sartori
1Department of Clinical and Biological Sciences, University of Turin, Turin, Italy. alberto.angeli@unito.it
Annals of the New York Academy of Sciences
|July 13, 2002
Summary
Interleukin-6 (IL-6) and IL-11 cytokines modulate glucocorticoid receptor (GR) binding in bone cells. IL-6 increases GR binding sites, while IL-11 decreases them, impacting osteoporosis development.
Area of Science:
- Endocrinology
- Cell Biology
- Bone Biology
Background:
- Glucocorticoid (GC)-induced osteoporosis is a common secondary form with unclear pathogenesis.
- While GC effects on cytokines are known, cytokine impact on GC action at target cells is less understood.
- Interleukin-6 (IL-6) and IL-11 are pro-resorptive cytokines promoting osteoclastogenesis.
Purpose of the Study:
- To investigate the effects of IL-6 and IL-11 on glucocorticoid receptor (GR) binding in human osteoblast-like cells.
- To explore the autocrine modulatory roles of IL-6 family cytokines on GRs in bone cells.
Main Methods:
- Utilized two human osteoblast-like cell lines (Saos-2 and MG-63).
- Employed radioligand binding assays and Scatchard analysis to determine GR binding.
- Assessed specific binding of type II GC receptors (GRs) after cytokine exposure.
Main Results:
- IL-6 was found to upregulate GR binding sites.
- IL-11 was observed to downregulate GR binding sites.
- GR affinity (Kd) remained unchanged by either cytokine.
Conclusions:
- IL-6 family cytokines exert autocrine modulatory effects on GRs in human osteoblast-like cells.
- Differential regulation of GR binding by IL-6 and IL-11 may contribute to bone loss dynamics in patients on GCs.
- Understanding these cytokine-GR interactions is crucial for managing GC-induced osteoporosis.