Okada Makiko, Ogasawara Hitoshi, Kaneko Hiroshi, Hishikawa Takashi, Sekigawa Iwao, Hashimoto Hiroshi, Maruyama Naoki, Kaneko Yutaro, Yamamoto Naoki
Department of Internal Medicine and Rheumatology, Juntendo Univeristy School of Medicine, Tokyo, Japan.
J Rheumatol. 2002 Aug;29(8):1678-82.
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.
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.
5-aza C increased clone 4-1-like messenger RNA in healthy controls, but not in patients with SLE.
Defects of methylation may contribute to the transcription of HERV in patients with SLE and this may be related to the pathogenesis of SLE.
我们最近报道，系统性红斑狼疮（SLE）患者中人类内源性逆转录病毒（HERV）克隆4-1样序列的转录增加。因此，我们研究了DNA甲基化在这种HERV转录中的作用。
使用逆转录聚合酶链反应（RT-PCR）和实时定量PCR检测去甲基化剂5-氮杂脱氧胞苷（5-aza C）对健康个体和SLE患者中HERV克隆4-1转录的影响。
5-aza C增加了健康对照中克隆4-1样信使核糖核酸（mRNA）的水平，但在SLE患者中未增加。
甲基化缺陷可能导致SLE患者中HERV的转录，这可能与SLE的发病机制有关。
