DOI: 10.1177/0961203309106181. Ultraviolet B exposure of peripheral blood mononuclear cells of patients with systemic lupus erythematosus inhibits DNA methylation

Ultraviolet B exposure of peripheral blood mononuclear cells of patients with systemic lupus erythematosus inhibits DNA methylation

10.1177/0961203309106181

Crossref journal-article

SAGE Publications

Lupus (179)

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease, in which sunlight (especially ultraviolet B (UVB) 290–320 nm) is known to induce exacerbation of disease. DNA methylation regulates gene expression, and hypomethylation is associated with abnormal cell function in SLE. The purpose of this study was to investigate the effect of UVB on DNA methylation in SLE and its significance in the pathogenesis of SLE. Forty-five patients with SLE and 20 healthy controls were enrolled in the study, which involved the investigation of DNA methylation and DNA methyltransferase 1 (DNMT1) of peripheral blood mononuclear cells with UVB irradiation. Our results demonstrate the following: The level of DNA methylation in patients with SLE was lower than that in the control group. DNA methylation was decreased after UVB irradiation at different dosages especially in patients with marlar rashes and leucopenia, but no significant difference was observed in the DNMT1 mRNA expression. DNA methylation levels in patients with active SLE were more sensitive to UVB. In conclusion, UVB exposure is able to inhibit DNA methylation, which subsequently takes part in the pathogenesis of SLE.

Bibliography

Wang, G., Zhang, M., Li, X., Zhang, H., Chen, W., Kan, M., & Wang, Y. (2009). Ultraviolet B exposure of peripheral blood mononuclear cells of patients with systemic lupus erythematosus inhibits DNA methylation. Lupus, 18(12), 1037â1044.

Authors 7

GS Wang (first)
M Zhang (additional)
XP Li (additional)
H Zhang (additional)
W Chen (additional)
M Kan (additional)
YM Wang (additional)

References 22 Referenced 29

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Dates

Type	When
Created	15 years, 11 months ago (Sept. 17, 2009, 6:08 a.m.)
Deposited	6 months, 1 week ago (Feb. 28, 2025, 6:06 p.m.)
Indexed	6 months ago (March 1, 2025, 1 a.m.)
Issued	15 years, 11 months ago (Sept. 17, 2009)
Published	15 years, 11 months ago (Sept. 17, 2009)
Published Online	15 years, 11 months ago (Sept. 17, 2009)
Published Print	15 years, 11 months ago (Oct. 1, 2009)

Funders 0

None

BibTeX

@article{Wang_2009, title={Ultraviolet B exposure of peripheral blood mononuclear cells of patients with systemic lupus erythematosus inhibits DNA methylation}, volume={18}, ISSN={1477-0962}, url={http://dx.doi.org/10.1177/0961203309106181}, DOI={10.1177/0961203309106181}, number={12}, journal={Lupus}, publisher={SAGE Publications}, author={Wang, GS and Zhang, M and Li, XP and Zhang, H and Chen, W and Kan, M and Wang, YM}, year={2009}, month=sep, pages={1037–1044} }

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  "abstract": "<jats:p> Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease, in which sunlight (especially ultraviolet B (UVB) 290\u2013320\u00a0nm) is known to induce exacerbation of disease. DNA methylation regulates gene expression, and hypomethylation is associated with abnormal cell function in SLE. The purpose of this study was to investigate the effect of UVB on DNA methylation in SLE and its significance in the pathogenesis of SLE. Forty-five patients with SLE and 20 healthy controls were enrolled in the study, which involved the investigation of DNA methylation and DNA methyltransferase 1 (DNMT1) of peripheral blood mononuclear cells with UVB irradiation. Our results demonstrate the following: The level of DNA methylation in patients with SLE was lower than that in the control group. DNA methylation was decreased after UVB irradiation at different dosages especially in patients with marlar rashes and leucopenia, but no significant difference was observed in the DNMT1 mRNA expression. DNA methylation levels in patients with active SLE were more sensitive to UVB. In conclusion, UVB exposure is able to inhibit DNA methylation, which subsequently takes part in the pathogenesis of SLE. </jats:p>",
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