Effect of total glucosides of peony on expression and DNA methylation status of ITGAL gene in CD4(+) T cells of systemic lupus erythematosus.
10.3969/j.issn.1672-7347.2012.05.006
- Author:
Ming ZHAO
1
;
Gongping LIANG
;
Shuangyan LUO
;
Qianjin LU
Author Information
1. Department of Dermatology, Central South University, Changsha, China.
- Publication Type:Journal Article
- MeSH:
CD11a Antigen;
genetics;
metabolism;
CD4-Positive T-Lymphocytes;
immunology;
metabolism;
DNA Methylation;
drug effects;
Down-Regulation;
drug effects;
Glucosides;
pharmacology;
Humans;
Lupus Erythematosus, Systemic;
genetics;
immunology;
Paeonia;
chemistry;
Promoter Regions, Genetic;
genetics;
RNA, Messenger;
genetics;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2012;37(5):463-468
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of total glucosides of peony (TGP) on expression and DNA methylation status of ITGAL gene (CD11a) in CD4(+) T cells from patients with systemic lupus erythematosus (SLE).
METHODS:CD4(+) T cells were isolated by positive selection using CD4 beads. CD4(+) T cells were treated by TGP at 0, 62.5, 312.5 and 1562.5 mg/L for 48 h. The MTT method was used to assess cell viability; mRNA expression level was measured by realtime-PCR; protein level of CD11a was measured by flow cytometric analysis; DNA methylation status was assayed by bisulfite sequencing.
RESULTS:No significant change in cell viability was found in CD4(+) T cells among the different concentration groups (P>0.05). Compared with control, the mRNA and protein levels of ITGAL were down-regulated significantly in SLE CD4(+) T cells treated with TGP (1562.5 mg/L) (P< 0.01). Furthermore, the extent of DNA methylation of ITGAL promoter was increased in TGP (1562.5 mg/L) treated CD4(+) T cells compared with control group (P<0.01).
CONCLUSION:TGP can repress CD11a gene expression through enhancing DNA methylation of ITGAL promoter in CD4(+) T cells from patients with SLE. This observation represents a preliminary step in understanding the mechanism of TGP in SLE therapy.
