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PPARgamma-2 and BMPR2 genes were differentially expressed in peripheral blood of SLE patients with osteonecrosis
Ching-Sheng Yeh1, Fu-Yen Chung, Chih-Ju Chen
1Department of Medical Research, School of Medical and Health Sciences, Fooyin University Hospital, Fooyin University, Kaohsiung Hsien, Taiwan, Republic of China.
Abstract:
Most researchers believe that the peroxisome proliferative activated receptor gamma (PPARgamma-2) and bone morphogenetic protein receptor type II (BMPR2) play important roles in steroid-induced osteonecrosis (ON). However, the molecular mechanism of this process is still unclear. Recent studies indicate that steroid treatments cause adipocyte formation due to differentiation of mesenchymal stem cells, which then prevents osteoblast formation. This study examined PPARgamma-2, bone morphogenetic protein 2 (BMP2), and BMPR2 in patients with systemic lupus erythromatosus (SLE) who eventually developed ON after prolonged steroid treatment. The subjects of this experiment included 220 SLE patients who had undergone steroid treatment for at least 2 years. Fifty-five of the 220 patients were ON patients, and 165 were non-ON patients. Real-time PCR was performed to analyze the expression of the PPARgamma-2, BMP2, and BMPR2 mRNA in the peripheral blood of these patients. The results indicated that the expression of PPARgamma-2 mRNA increased 37% in the ON patients' peripheral blood, but the expression of BMPR2 mRNA decreased 57%. The average expression of the PPARgamma-2 mRNA in the ON patients was significantly higher than that in the non-ON patients (p = 0.044). Conversely, the expression of BMPR2 mRNA was significantly lower than that in non-ON patients (p = 0.036), but the expression of BMP2 mRNA did not significantly differ. This study demonstrated that the PPARgamma-2 and BMPR2 have important roles in the ON process after prolonged steroid administration in SLE patients; however, the detailed molecular mechanisms of this process require further study.
Insights
Steroid-induced osteonecrosis (ON) in SLE patients involves altered gene expression. PPARgamma-2 levels increased, while BMPR2 levels decreased, suggesting roles in ON development.
Area of Science:
- Molecular Biology
- Genetics
- Rheumatology
Background:
- Steroid-induced osteonecrosis (ON) is a complication of prolonged corticosteroid therapy, particularly in systemic lupus erythematosus (SLE) patients.
- The roles of peroxisome proliferative activated receptor gamma 2 (PPARgamma-2) and bone morphogenetic protein receptor type II (BMPR2) in ON are suspected but not fully understood.
- Steroids may promote adipocyte differentiation from mesenchymal stem cells, hindering osteoblast formation and contributing to ON.
Purpose of the Study:
- To investigate the expression levels of PPARgamma-2, bone morphogenetic protein 2 (BMP2), and BMPR2 in SLE patients with and without steroid-induced ON.
- To explore the potential molecular mechanisms linking these genes to the development of ON following long-term steroid treatment.
Main Methods:
- A case-control study involving 220 SLE patients (55 with ON, 165 without ON) who received steroid treatment for at least two years.
- Real-time quantitative polymerase chain reaction (RT-qPCR) was used to measure the mRNA expression levels of PPARgamma-2, BMP2, and BMPR2 in peripheral blood samples.
Main Results:
- PPARgamma-2 mRNA expression was significantly higher (37% increase) in SLE patients with ON compared to those without ON (p = 0.044).
- BMPR2 mRNA expression was significantly lower (57% decrease) in SLE patients with ON compared to those without ON (p = 0.036).
- No significant difference in BMP2 mRNA expression was observed between the ON and non-ON groups.
Conclusions:
- PPARgamma-2 and BMPR2 play significant roles in the pathogenesis of steroid-induced ON in SLE patients.
- The observed alterations in PPARgamma-2 and BMPR2 expression suggest their involvement in the molecular pathways leading to ON.
- Further research is warranted to elucidate the precise molecular mechanisms underlying the involvement of PPARgamma-2 and BMPR2 in ON.