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Improving the development of early bovine somatic‐cell nuclear transfer embryos by treating adult donor cells with vitamin C
Author(s) -
Chen Huanhuan,
Zhang Lei,
Guo Zekun,
Wang Yongsheng,
He Rongjun,
Qin Yumin,
Quan Fusheng,
Zhang Yong
Publication year - 2015
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.22531
Subject(s) - somatic cell nuclear transfer , biology , blastocyst , somatic cell , andrology , embryo , reprogramming , cell growth , sox2 , dna methylation , inner cell mass , cell , microbiology and biotechnology , methylation , immunology , embryonic stem cell , embryogenesis , biochemistry , gene expression , dna , gene , medicine
SUMMARY Vitamin C (Vc) has been widely studied in cell and embryo culture, and has recently been demonstrated to promote cellular reprogramming. The objective of this study was to identify a suitable Vc concentration that, when used to treat adult bovine fibroblasts serving as donor cells for nuclear transfer, improved donor‐cell physiology and the developmental potential of the cloned embryos that the donor nuclei were used to create. A Vc concentration of 0.15 mM promoted cell proliferation and increased donor‐cell 5‐hydroxy methyl cytosine levels 2.73‐fold ( P  < 0.05). The blastocyst rate was also significantly improved after nuclear transfer (39.6% treated vs. 26.0% control, P  < 0.05); the average number of apoptotic cells in cloned blastocysts was significantly reduced (2.2 vs. 4.4, P  < 0.05); and the inner cell mass‐to‐trophectoderm ratio (38.25% vs. 30.75%, P  < 0.05) and expression of SOX2 (3.71‐fold, P  < 0.05) and POU5F1 (3.15‐fold, P  < 0.05) were significantly increased. These results suggested that Vc promotes cell proliferation, decreases DNA methylation levels in donor cells, and improves the developmental competence of bovine somatic‐cell nuclear transfer embryos. Mol. Reprod. Dev. 82: 867–879, 2015. © 2015 Wiley Periodicals, Inc .

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