Thin endometrium transcriptome analysis reveals a potential mechanism of implantation failure.
Thin endometrium transcriptome analysis reveals a potential mechanism of implantation failure.
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DOI：
10.1002/rmb2.12030
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发表时间：
2017-04
影响因子：
3.4
通讯作者：
Sugino N
中科院分区：
文献类型：
--
作者：
Maekawa R;Taketani T;Mihara Y;Sato S;Okada M;Tamura I;Jozaki K;Kajimura T;Asada H;Tamura H;Takasaki A;Sugino N
虽然薄的子宫内膜已被公认为是着床失败的关键因素，但关于其分子机制的信息很少。本研究通过使用全基因组mRNA表达分析来研究这些机制。在月经周期的黄体中期，从总共6名女性中获得薄且正常的子宫内膜组织。用微阵列分析转录组。根据基因本体（GO）术语和京都基因和基因组百科全书（KEGG）途径对差异表达的基因进行分类。与对照子宫内膜相比，该研究在薄子宫内膜中确定了318个上调基因和322个下调基因。GO和KEGG通路分析表明，薄的子宫内膜具有异常激活的免疫和自然杀伤细胞的细胞毒性，伴随着炎性细胞因子（如IFN-γ）数量的增加。与代谢和抗氧化应激相关的各种基因在薄的子宫内膜中下调。薄子宫内膜的着床失败似乎与异常激活的炎症环境和异常降低的氧化应激反应有关。
Although a thin endometrium has been well recognized as a critical factor in implantation failure, little information is available regarding the molecular mechanisms. The present study investigated these mechanisms by using genome‐wide mRNA expression analysis. Thin and normal endometrial tissue was obtained from a total of six women during the mid‐luteal phase of the menstrual cycle. The transcriptomes were analyzed with a microarray. Differentially expressed genes were classified according to Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The study identified 318 up‐regulated genes and 322 down‐regulated genes in the thin endometrium, compared to the control endometrium. The GO and KEGG pathway analyses indicated that the thin endometrium possessed aberrantly activated immunity and natural killer cell cytotoxicity that was accompanied by an increased number of inflammatory cytokines, such as IFN‐γ. Various genes that were related to metabolism and anti‐oxidative stress were down‐regulated in the thin endometrium. Implantation failure in the thin endometrium appears to be associated with an aberrantly activated inflammatory environment and aberrantly decreased response to oxidative stress.