Thin endometrium transcriptome analysis reveals a potential mechanism of implantation failure. (9th April 2017)

• Record Type: Journal Article
• Authors: Maekawa, Ryo; Taketani, Toshiaki; Mihara, Yumiko; Sato, Shun; Okada, Maki; Tamura, Isao; Jozaki, Kosuke; Kajimura, Takuya; Asada, Hiromi; Tamura, Hiroshi; Takasaki, Akihisa; Sugino, Norihiro
• Is Part Of: Reproductive medicine and biology. Volume 16:Number 2(2017)
• Page Start: 206
• Page End: 227
• Publication Date: 2017-04-09
• Subjects: implantation failure -- infertility -- oxidative stress -- thin endometrium -- uterine natural killer cells; Reproduction -- Periodicals; Reproductive health -- Periodicals; 612.6
• DOI: 10.1002/rmb2.12030
• Languages: English
• ISSNs: 1445-5781

Abstract

Abstract: Aim: 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. Methods: 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. Results: 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. Conclusion: Implantation failure in the thin endometrium appears to be associated with an aberrantly activated inflammatory environment and aberrantly decreased response to oxidative stress.