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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, METHODS, METHODS, METHODS, METHODS, RESULTS. Meshes: Animals, DNA Methylation, Embryo, Mammalian, Female, Genomic Imprinting, Kruppel-Like Transcription Factors, Male, Mice, Mice, Inbred C57BL, Nuclear Proteins, Oocytes, Ovulation, RNA, Long Noncoding, RNA, Untranslated, Reproductive Techniques, Assisted, Superovulation.
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Do embryonic imprinting perturbations originate from superovulation-induced defects in DNA methylation acquisition? Context: To investigate whether superovulation disrupts maternal imprint acquisition in oocytes. Animal model. Academic institute. Spontaneously ovulated and superovulated mice. Low and high hormone dosage treatments were administered to females, and ovulated metaphase II oocytes were collected. Imprinted DNA methylation was analyzed at Snrpn, Kcnq1ot1, Peg3, and H19 in individual oocytes. Examination of 125 individual oocytes derived from females subjected to low and high hormone treatments revealed normal imprinted methylation patterns that were comparable to oocytes derived from spontaneously ovulated females.
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Maternal imprint acquisition was not affected by superovulation. Given its aberrant effects during preimplantation development, superovulation must instead disrupt maternal-effect gene products that are required after fertilization for imprint maintenance. These results eliminate imprint acquisition per se as the initial stage of imprint loss and point to the importance of analyses on early embryos after procedures involving oocyte manipulation. Final Decision: no