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Published on: August 11, 2023
Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH
Huihui Xu1,2,3, Qinghe Zeng1,2,3, Kaiao Zou1,2,3
1The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, 310006, China.
Background:
This study aimed to investigate the pathogenic factors of glucocorticoids (GCs)-induced osteonecrosis of the femoral head (GONFH) and its underlying pathogenesis in vivo and in vitro.
Methods:
Radiographical (µCT) scanning, histopathological, immunohistochemical, reactive oxygen species (ROS) and tunel staining were conducted on GONFH patients and rats. ROS, tunel, flow cytometry, alkaline phosphatase, Oil red O staining, reverse transcription‑quantitative PCR and western blotting were applied to elucidate the exact pathogenesis mechanism.
Results:
Clinical and animal studies demonstrated increased levels of ROS, aggravated oxidative stress (OS) microenvironment, augmented apoptosis and imbalance in osteogenic/lipogenic in the GONFH group compared to the control group. The fate of mesenchymal stem cells (MSCs) directed by GCs is a crucial factor in determining GONFH. In vitro studies further revealed that GCs promote excessive ROS production through the expression of NOX family proteins, leading to a deterioration of the OS microenvironment in MSCs, ultimately resulting in apoptosis and imbalance in osteogenic/lipogenic differentiation. Furthermore, our results confirmed that the NOX inhibitor-diphenyleneiodonium chloride and the NF-κB inhibitor-BAY 11-7082 ameliorated apoptosis and osteogenic/lipogenic differentiation imbalance of MSCs induced by an excess of GCs.
Conclusion:
We demonstrated for the first time that the aggravation of the OS microenvironment in MSCs caused by high doses of GCs leading to apoptosis and differentiation imbalance is a crucial factor in the pathogenesis of GONFH, mediated through activating the NOX/ROS/NF-κB signaling pathway.
Insights
Glucocorticoids (GCs) induce femoral head osteonecrosis by promoting oxidative stress in mesenchymal stem cells (MSCs). This pathway, involving NOX/ROS/NF-κB, leads to cell death and differentiation imbalance, contributing to GONFH pathogenesis.
Area of Science:
- Biomedical research
- Cell biology
- Pathogenesis studies
Background:
- Glucocorticoids (GCs) are associated with osteonecrosis of the femoral head (GONFH).
- The precise mechanisms underlying GC-induced GONFH require further elucidation.
- Understanding the role of mesenchymal stem cells (MSCs) in this process is critical.
Purpose of the Study:
- To investigate the pathogenic factors and underlying mechanisms of glucocorticoids (GCs)-induced osteonecrosis of the femoral head (GONFH).
- To explore the role of oxidative stress and MSCs in GC-induced bone damage.
- To identify potential therapeutic targets for GONFH.
Main Methods:
- In vivo and in vitro studies using GONFH patients and rat models.
- Utilized techniques including µCT scanning, histopathology, immunohistochemistry, ROS and TUNEL staining.
- Employed flow cytometry, gene expression (RT-qPCR), and protein analysis (Western blotting) to assess cellular mechanisms.
Main Results:
- GCs significantly increased reactive oxygen species (ROS) and aggravated oxidative stress (OS) in MSCs.
- GCs promoted MSC apoptosis and an imbalance in osteogenic/lipogenic differentiation.
- NOX family proteins were identified as key mediators of ROS production by GCs.
Conclusions:
- GCs induce GONFH by promoting an OS microenvironment in MSCs via the NOX/ROS/NF-κB pathway.
- This leads to MSC apoptosis and impaired differentiation, crucial factors in GONFH pathogenesis.
- Inhibitors of NOX and NF-κB show potential in ameliorating GC-induced MSC damage.
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