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ArtikelDeoxyribonucleic acid methyltransferases and methyl-CpG-binding domain proteins in human endometrium and endometriosis  
Oleh: Kaam, Kim J.A.F. van ; Delvoux, Bert ; Romano, Andrea ; D’Hooghe, T. ; Dunselman, Gerard A.J. ; Groothuis, Patrick G.
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 95 no. 04 (Mar. 2011), page 1421-1427.
Topik: ENDOMETRIUM; Endometriosis; endometrium; DNA methylation; epigenetics; DNMT; MBD
Ketersediaan
  • Perpustakaan FK
    • Nomor Panggil: F02.K.2011.03
    • Non-tandon: 1 (dapat dipinjam: 0)
    • Tandon: tidak ada
    Lihat Detail Induk
Isi artikelObjective To determine [1] expression levels of both DNA methyltransferases (DNMTs) and methyl-CpG-binding domain proteins (MBDs) in human endometrium throughout the menstrual cycle and in eutopic and ectopic endometrium of patients with endometriosis and [2] hormone responsiveness of DNMT and MBD expression in explant cultures of proliferative phase endometrium. Design In vitro study. Setting Academic medical center. Patient(s) Premenopausal women with and without endometriosis. Intervention(s) Explant cultures of proliferative phase endometrium were treated with vehicle, 17ß-E2, or a combination of E2 and P (E2 + P) for 24 hours. Main Outcome Measure(s) Expression levels of DNMT1, DNMT2, and DNMT3B and MBD1, MBD2, and MeCP2 with use of real-time quantitative polymerase chain reaction. Result(s) Expression levels of DNMT1 and MBD2 were significantly higher in secretory-phase endometrium compared with proliferative endometrium and menstrual endometrium. In explant cultures, treatment with E2 + P resulted in significant up-regulation of DNMT1 and MBD2. Expression levels of several DNMTs and MBDs were significantly lower in endometriotic lesions compared with eutopic endometrium of women with endometriosis and disease-free controls. Conclusion(s) These findings suggest a role for DNMTs and MBDs in the growth and differentiation of the human endometrium and support the notion that endometriosis may be an epigenetic disease
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