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- W2116159182 abstract "The in vitro production of mammalian embryos suffers from high frequencies of developmental failure due to excessive levels of permanent embryo arrest and apoptosis caused by oxidative stress. The p66Shc stress adaptor protein controls oxidative stress response of somatic cells by regulating intracellular ROS levels through multiple pathways, including mitochondrial ROS generation and the repression of antioxidant gene expression. We have previously demonstrated a strong relationship with elevated p66Shc levels, reduced antioxidant levels and greater intracellular ROS generation with the high incidence of permanent cell cycle arrest of 2-4 cell embryos cultured under high oxygen tensions or after oxidant treatment. The main objective of this study was to establish a functional role for p66Shc in regulating the oxidative stress response during early embryo development. Using RNA interference in bovine zygotes we show that p66Shc knockdown embryos exhibited increased MnSOD levels, reduced intracellular ROS and DNA damage that resulted in a greater propensity for development to the blastocyst stage. P66Shc knockdown embryos were stress resistant exhibiting significantly reduced intracellular ROS levels, DNA damage, permanent 2-4 cell embryo arrest and diminished apoptosis frequencies after oxidant treatment. The results of this study demonstrate that p66Shc controls the oxidative stress response in early mammalian embryos. Small molecule inhibition of p66Shc may be a viable clinical therapy to increase the developmental potential of in vitro produced mammalian embryos." @default.
- W2116159182 created "2016-06-24" @default.
- W2116159182 creator A5049942575 @default.
- W2116159182 creator A5071432046 @default.
- W2116159182 creator A5083155937 @default.
- W2116159182 date "2014-01-24" @default.
- W2116159182 modified "2023-09-24" @default.
- W2116159182 title "The p66Shc Adaptor Protein Controls Oxidative Stress Response in Early Bovine Embryos" @default.
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- W2116159182 doi "https://doi.org/10.1371/journal.pone.0086978" @default.
- W2116159182 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3901717" @default.
- W2116159182 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24475205" @default.
- W2116159182 hasPublicationYear "2014" @default.
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