Abstract
Objective:
We recently reported that transcription of human endogenous retrovirus (HERV) clone 4-1-like sequences is increased in patients with systemic lupus erythematosus (SLE). We therefore investigated the role of DNA methylation in the transcription of this HERV.
Methods:
The effect of a demethylating agent, 5-aza-deoxycytidine (5-aza C), on the transcription of HERV clone 4-1 in healthy individuals and patients with SLE was examined using reverse transcriptase-PCR and real-time quantitative PCR.
Results:
5-aza C increased clone 4-1-like messenger RNA in healthy controls, but not in patients with SLE.
Conclusion:
Defects of methylation may contribute to the transcription of HERV in patients with SLE and this may be related to the pathogenesis of SLE.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Azacitidine / analogs & derivatives*
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Azacitidine / pharmacology
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Cells, Cultured
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Clone Cells / drug effects
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Clone Cells / metabolism
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DNA Methylation*
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DNA Primers / chemistry
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Decitabine
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Endogenous Retroviruses / genetics*
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Endogenous Retroviruses / metabolism
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Endogenous Retroviruses / pathogenicity
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Female
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Gene Products, gag / genetics
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Gene Products, gag / metabolism
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Humans
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Leukocytes, Mononuclear / drug effects
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Leukocytes, Mononuclear / metabolism
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Lupus Erythematosus, Systemic / blood
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Lupus Erythematosus, Systemic / virology*
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Middle Aged
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RNA, Messenger / analysis
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RNA, Viral / analysis
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Reverse Transcriptase Polymerase Chain Reaction
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Transcription, Genetic*
Substances
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DNA Primers
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Gene Products, gag
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RNA, Messenger
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RNA, Viral
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Decitabine
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Azacitidine