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Aberrant Expression of Mir-29A/29B and Methylation Level of Mouse Embryos After in Vitro Fertilization and Vitrification at Two-Cell Stage Publisher Pubmed



Movahed E1 ; Soleimani M1, 2 ; Hosseini S3 ; Akbari Sene A4 ; Salehi M3, 5
Authors
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Authors Affiliations
  1. 1. Department of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  4. 4. IVF Department, Shahid Akbar-Abadi Hospital IVF Center, Iran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Journal of Cellular Physiology Published:2019


Abstract

Proper epigenetic modifications during preimplantation embryo development are important for a successful pregnancy. We aim to investigate the putative influence of in vitro fertilization (IVF) and vitrification on DNA methylation in mouse preimplantation embryos. The study groups consisted of blastocyst-derived vitrified two-cell embryos, nonvitrified embryos, and a control group of in vivo derived blastocysts. We assessed developmental competence, global DNA methylation, relative expression levels of miR-29a/29b, and their target genes, Dnmt3a/3b. Vitrified embryos had a lower developmental rate as compared with nonvitrified embryos. There was no significant decrease in blastocyst cell numbers among studied groups, whereas there was a steady decline in DNA methylation after IVF and vitrification. The levels of miR-29a/29b upregulated in the experimental groups as compared with the control group. IVF and vitrification caused Dnmt3a/3b downregulations in blastocysts. The results of this study have suggested that a relationship exists between IVF and embryo vitrification with methylation interruptions in the blastocysts. © 2019 Wiley Periodicals, Inc.