Embryonic defects induced by maternal obesity in mice derive from Stella insufficiency in oocytes

Han, Longsen; Ren, Chao; Li, Ling; Li, Xiaoyan; Ge, Juan; Wang, Haichao; Miao, Yi; Guo, Xuejiang; Moley, Kelle H.; Shu, Wenjie; Wei, Qiang

doi:10.1038/s41588-018-0055-6

Cited by 118 publications

(108 citation statements)

References 61 publications

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“…Immunofluorescence staining was performed as previously described . Embryos were incubated in pronase to remove the zona pellucida and mucin coat.…”

Section: Methodsmentioning

confidence: 99%

“…Immunofluorescence staining was performed as previously described. 29 Embryos were incubated in pronase to remove the zona pellucida and mucin coat. For 5-methylcytosine (5-mC) immunostaining, embryos were fixed in 4% paraformaldehyde/ PBS for 30 minutes, incubated in 4 mol/L HCl solution for 10 minutes, and neutralized in Tris-HCl solution (pH 8.0) for 10 minutes.…”

Section: Immunofluorescencementioning

confidence: 99%

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Extracellular vesicles and melatonin benefit embryonic develop by regulating reactive oxygen species and 5‐methylcytosine

Luo

et al. 2020

Journal of Pineal Research

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Embryo culture conditions are crucial as they can affect embryo quality and even offspring. Oviductal extracellular vesicles (EVs) long been considered a major factor influencing interactions between the oviduct and embryos, and thus its absence is associated with inferior embryonic development in in vitro culture. Herein, we demonstrated that melatonin is present in oviduct fluids and oviduct fluid‐derived EVs. Addition of either EVs (1.87 × 1011 particles/mL) or melatonin (340 ng/mL) led to a significant downregulation of reactive oxygen species (ROS) and 5‐methylcytosine (5‐mC), as well as an increase in the blastocyst rate of embryos, which was inhibited by the addition of luzindole—a melatonin receptor agonist. A combination of EVs (1.87 × 1010 particles/mL) and melatonin (at 34.3 pg/mL) led to the same results as well as a significant decrease in the apoptosis index and increase in the inner cell mass (ICM)/trophectoderm (TE) index. These results suggest that an EV‐melatonin treatment benefits embryonic development. Our findings provide insights into the role of EVs and melatonin during cell communication and provide new evidence of the communication between embryos and maternal oviduct.

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“…Immunofluorescence staining was performed as previously described . Embryos were incubated in pronase to remove the zona pellucida and mucin coat.…”

Section: Methodsmentioning

confidence: 99%

Section: Immunofluorescencementioning

confidence: 99%

Extracellular vesicles and melatonin benefit embryonic develop by regulating reactive oxygen species and 5‐methylcytosine

Luo

et al. 2020

Journal of Pineal Research

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“…Fluorescence intensity was assessed as we described previously (Han et al, ). When quantifying ROS signal, a Z‐stack of oocyte was taken, and images were used to generate a projection containing all ROS signals.…”

Section: Methodsmentioning

confidence: 99%

NMNAT2‐mediated NAD⁺ generation is essential for quality control of aged oocytes

Zeng

et al. 2019

Aging Cell

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Advanced maternal age has been reported to impair oocyte quality; however, the underlying mechanisms remain to be explored. In the present study, we identified the lowered NAD+ content and decreased expression of NMNAT2 protein in oocytes from old mice. Specific depletion of NMNAT2 in mouse oocytes disturbs the meiotic apparatus assembly and metabolic activity. Of note, nicotinic acid supplementation during in vitro culture or forced expression of NMNAT2 in aged oocytes was capable of reducing the reactive oxygen species (ROS) production and incidence of spindle/chromosome defects. Moreover, we revealed that activation or overexpression of SIRT1 not only partly prevents the deficient phenotypes of aged oocytes but also ameliorates the meiotic anomalies and oxidative stress in NMNAT2‐depleted oocytes. To sum up, our data indicate a role for NMNAT2 in controlling redox homeostasis during oocyte maturation and uncover that NMNAT2‐ NAD+‐SIRT1 is an important pathway mediating the effects of maternal age on oocyte developmental competence.

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“…The second-round PCR products were subcloned, and $10 clones for each sample were sequenced. The percentage of methylation was calculated as 100 3 (number of methylated CpG dinucleotides)/ (total number of CpGs) as previously described by Han et al (26).…”

Section: Bisulfite Sequencingmentioning

confidence: 99%

Deletion of maternal UHRF1 severely reduces mouse oocyte quality and causes developmental defects in preimplantation embryos

Cao

Liu

et al. 2019

FASEB j.

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The ubiquitin‐like, containing PHD and RING finger domains, 1 (UHRF1) protein recognizes DNA methylation and histone modification and plays a critical role in epigenetic regulation. Recently, UHRF1 was shown to have a role in DNA methylation in oocytes and early embryos. Here, we reveal that maternal UHRF1 determines the quality of mouse oocytes. We generated oocyte‐specific Uhrf1‐knockout mice and found that females were sterile, and few maternal UHRF1‐null embryos developed into blastocysts. The UHRF1‐null oocytes had an increased incidence of aneuploidy and DNA damage. In addition to defective DNA methylation, histone modification was affected during oogenesis, with UHRF1‐null germinal vesicle and metaphase II‐stage oocytes exhibiting reduced global histone H3 lysine 9 dimethylation levels and elevated acetylation of histone H4 lysine 12. Taken together, our results suggest that UHRF1 plays an important role in determining oocyte quality and affects epigenetic regulation of oocyte maturation as a maternal protein, which is crucial for embryo developmental potential. Further exploration of the biologic function and underlying mechanisms of maternal UHRF1 will enhance our understanding of the maternal control of the oocyte and early embryonic development.—Cao, Y., Li, M., Liu, F., Ni, X., Wang, S., Zhang, H., Sui, X., Huo, R. Deletion of maternal UHRF1 severely reduces mouse oocyte quality and causes developmental defects in preimplantation embryos. FASEB J. 33, 8294–8305 (2019). http://www.fasebj.org

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Embryonic defects induced by maternal obesity in mice derive from Stella insufficiency in oocytes

Cited by 118 publications

References 61 publications

Extracellular vesicles and melatonin benefit embryonic develop by regulating reactive oxygen species and 5‐methylcytosine

Extracellular vesicles and melatonin benefit embryonic develop by regulating reactive oxygen species and 5‐methylcytosine

NMNAT2‐mediated NAD⁺ generation is essential for quality control of aged oocytes

Deletion of maternal UHRF1 severely reduces mouse oocyte quality and causes developmental defects in preimplantation embryos

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Embryonic defects induced by maternal obesity in mice derive from Stella insufficiency in oocytes

Cited by 118 publications

References 61 publications

Extracellular vesicles and melatonin benefit embryonic develop by regulating reactive oxygen species and 5‐methylcytosine

Extracellular vesicles and melatonin benefit embryonic develop by regulating reactive oxygen species and 5‐methylcytosine

NMNAT2‐mediated NAD+ generation is essential for quality control of aged oocytes

Deletion of maternal UHRF1 severely reduces mouse oocyte quality and causes developmental defects in preimplantation embryos

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NMNAT2‐mediated NAD⁺ generation is essential for quality control of aged oocytes