CpG Oligodeoxynucleotides Downregulate Placental Adiponectin and Increase Embryo Loss in Non-Obese Diabetic Mice.
CpG Oligodeoxynucleotides Downregulate Placental Adiponectin and Increase Embryo Loss in Non-Obese Diabetic Mice.
复制标题
CpG 寡脱氧核苷酸下调胎盘脂联素并增加非肥胖糖尿病小鼠的胚胎损失。
DOI：
10.1111/aji.12515
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发表时间：
2016-07
期刊：
影响因子：
--
通讯作者：
Lin Y
中科院分区：
文献类型：
--
作者：
Qin CM;Tian FJ;Liu XR;Wu F;Ma XL;Lin Y
CpG寡脱氧核苷酸（CpG oligodeoxynucleotides，ODNs）可诱导非肥胖糖尿病（non-obese diabetic，NOD）小鼠的免疫功能改变，增加胚胎丢失率，但其机制尚不清楚。本研究旨在确定脂联素在CpG ODN诱导的妊娠失败中的作用。NOD小鼠腹腔注射1826寡核苷酸，ODN 2216、ODN 2006和ODN 2395刺激人滋养层细胞系，研究脂联素表达模式及其对滋养层功能的可能影响。CpG ODNs通过cJun N末端激酶信号通路下调脂联素，导致胚胎丢失率增加（从6.9%增加到33.3%）。ODN 2006损害人类滋养层细胞迁移，脂联素治疗成功挽救了该细胞迁移。CpG ODNs降低NOD小鼠胎盘脂联素的表达，损害人类滋养层功能，并与胚胎丢失增加有关。因此，脂联素可能在预防细菌引起的妊娠失败中发挥重要的保护作用。
CpG oligodeoxynucleotides (ODNs) can induce immunological changes in non‐obese diabetic (NOD) mice and increase embryo loss, but little is known about the mechanism. This study aimed to determine the role of adiponectin in CpG ODN‐induced pregnancy failure. Oligodeoxynucleotide 1826 was intraperitoneally injected to NOD mice, and ODN 2216, ODN 2006, and ODN 2395 were used to stimulate human trophoblast cell lines to investigate adiponectin expression patterns and its possible effects on trophoblast function. CpG ODNs downregulated adiponectin via the cJun N‐terminal kinase signaling pathway and led to increased embryo loss (from 6.9 to 33.3%). ODN 2006 impaired human trophoblast cell migration, which was successfully rescued by adiponectin treatment. CpG ODNs decreased placental adiponectin expression in NOD mice and impaired human trophoblast function and was associated with increased embryo loss. Adiponectin may therefore play an important protective role in the prevention of bacteria‐induced pregnancy failure.
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