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Maternal obesity in mice not only affects fresh embryo quality but also aggravates injury due to vitrification
Wenhong Ma1, Xingfang Huang2, Xing Yang2
1Reproductive Centre of Liuzhou Municipal Maternity and Child Healthcare Hospital, Liuzhou, 545000, People's Republic of China.
Purpose:
The aims of the present study are to identify the mechanism(s) whereby obesity impairs fresh embryos and to clarify the effects of vitrification on lipid droplet content within embryos from maternally obese mice.
Methods:
The diet-induced obesity mouse model was established, and the zygotes were captured and cultured to day 3. The eight-cell embryos were selected and divided into fresh and vitrified groups. The blastocysts derived from fresh embryos were used as a control. The expression profiles of endoplasmic reticulum (ER) stress genes (Atf4, Grp78, and Hsp70) and other genes (MnSOD, p53, Gadd45g, caspase-3, IGF-II, ZO-1, and E-cadherin) on day-3 fresh and post-warming eight-cell embryos from obese and control groups were determined. For day-5 fresh blastocysts and blastocysts previously vitrified on day 3, the expression profiles for all of the above genes were also determined.
Results:
For the fresh group, obesity significantly upregulated Hsp70, p53, IGF-II, and ZO-1 expression in embryos on day 3 and notably upregulated Atf4, MnSOD, Gadd45g, caspase-3, ZO-1, and E-cadherin expression in blastocysts on day 5. For vitrified ones, obesity significantly upregulated Atf4, MnSOD, and Gadd45g expression in embryos on day 3 and notably upregulated Hsp70 expression and downregulated MnSOD in day 5 blastocysts previously vitrified on day 3.
Conclusions:
Obesity impairs fresh embryos and aggravates embryonic vitrification injury at a molecular level.
