Role of Olf-1/EBF associated zinc finger protein gene in bone marrow mesenchymal stem cells of systemic lupus erythematosus patients
10.3760/cma.j.issn.1007-7480.2012.06.002
- VernacularTitle:Olf-1/EBF相关锌指蛋白基因在系统性红斑狼疮患者骨髓间充质干细胞中作用机制的研究
- Author:
Yan LIU
;
Xiaolei MA
;
Jing HUANG
;
Lingyun SUN
;
Xuebing FENG
- Publication Type:Journal Article
- Keywords:
Lupus erythematosus,systemic;
Mesenchymal stem cells;
Olf-1/EBF associated zinc finger protein;
Chemokine (C-C motif) ligand 2
- From:
Chinese Journal of Rheumatology
2012;16(6):364-367
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the role of OIf-1/EBF associated zinc finger protein (OAZ),a transcription factor encoded by a positional systemic lupus erythematosus (SLE) candidate gene,in the function of mesenchymal stem cells (MSC) of SLE patients by silencing this gene.Methods OAZ mRNA levels of bone marrow MSC obtained from 5 SLE patients and 5 healthy controls were detected by real-time PCR.Bone marrow MSC obtained from 6 SLE patients were incubated with specific siRNAs for 3 days,then cells were harvested for OAZ measurement,Idl-3 and CCL2 mRNA levels were tested by real-time PCR,and levels of CCL2 were detected in culture supernatants using ELISA.Differences between groups were analyzed using t-test or MannWhitney test.Results ① OAZ mRNA levels of bone marrow MSC were significantly elevated in SLE patients (0.013±0.016) compared to healthy controls (0.001±0.000,P=0.009).② After OAZ silencing,the expression levels of OAZ,Id1,Id2 and ld3 mRNA were significantly decreased (△Ct 10.3±0.7,15.2±1.6,8.1±1.4,10.5±0.6 vs 8.7±0.7,14.1±1.2,7.1±1.5,9.8±0.6) (P all ＜0.05).③ Both the expression levels of CCL2 mRNA (△Ct 2.2±1.1 vs 3.0±1.1 ) and the levels of CCL2 protein in culture supernatants [(341±29) pg/ml vs (304±19) pg/ml] were significantly increased in OAZ silencing group comparing to those in the control group (P all ＜0.05).Conclusion OAZ gene expression is significantly elevated in bone marrow MSC of SLE patients.OAZ may affect autoantibody production in SLE patients by regulating CCL2 expression.
