ArticleReproductive sciences (Thousand Oaks, Calif.)2026
Evaluation of the DNA Repair Mechanism Following In Vitro Maturation of Mouse Oocytes.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Infertility is a common clinical condition, and in vitro maturation (IVM) of oocytes plays a critical role in fertility preservation and assisted reproductive technologies (ART). DNA repair mechanisms are crucial for maintaining genomic stability in oocytes and supporting embryo development. This study investigated the expression of key DNA repair genes during IVM and compared the findings with in vivo-matured oocytes. Adult female mice were administered pregnant mare serum gonadotropin to stimulate follicular growth. Oocytes were collected and categorized into two groups: IVM and in vivo-matured. Quantitative reverse transcription PCR was used to assess the expression levels of H2afx, Atm, Nbs1, Mre11, Rad50, and Rad51, with B2m as the reference gene. The maturation rate to metaphase II (MII) was significantly lower in IVM oocytes compared with in vivo-matured oocytes (p < 0.001), representing a key deficit in developmental competence. DNA repair gene expression was markedly downregulated in IVM-matured oocytes, with Mre11 showing the largest reduction (0.11 ± 0.01-fold, P < 0.0001). H2afx was reduced (0.28 ± 0.15-fold, P = 0.01), but this difference did not remain significant after multiple-testing correction. The primary finding of this study is that IVM results in a significant deficit in fully matured MII oocytes, which is associated with impaired expression of DNA repair genes. These deficiencies likely underlie the reduced developmental competence observed in IVM-derived embryos. Refining IVM protocols to support genomic integrity may improve ART outcomes.
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