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.
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Authors | Ming Zhao, Gongping Liang, Shuangyan Luo, Qianjin Lu |
Journal | Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
(Zhong Nan Da Xue Xue Bao Yi Xue Ban)
Vol. 37
Issue 5
Pg. 463-8
(May 2012)
ISSN: 1672-7347 [Print] China |
PMID | 22659657
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- CD11a Antigen
- Glucosides
- RNA, Messenger
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Topics |
- 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)
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