Related Experiment Video

Updated: Mar 8, 2026

Author Spotlight: Advancing Therapeutic Strategies for Improving Pregnancy Rates by Analyzing Embryo-Endometrium Interactions
05:13

Author Spotlight: Advancing Therapeutic Strategies for Improving Pregnancy Rates by Analyzing Embryo-Endometrium Interactions

Published on: June 21, 2024

1.9K

Effect of potential role of p53 on embryo development arrest induced by H2O2 in mouse

De-Bao Hu1, Zhong-Shu Li1, Ihsan Ali1

  • 1Laboratory of Animal Genetic Breeding and Reproduction, Agricultural College of Yanbian University, Yanji, 133002, China.

In Vitro Cellular & Developmental Biology. Animal
|January 28, 2017
PubMed

Insights

Oxidative stress causes embryonic development arrest by activating tumor suppressor p53. This study reveals how reactive oxygen species (ROS) impact p53 and downstream genes, affecting early mammalian embryo development in vitro.

Area of Science:

  • Reproductive Biology
  • Cellular Stress Response
  • Developmental Biology

Background:

  • Oxidative stress is implicated in mammalian embryo development arrest in vitro, but the precise mechanisms remain unclear.
  • The tumor suppressor protein p53 plays a critical role in cell cycle regulation and programmed cell death.
  • Emerging evidence links reactive oxygen species (ROS) levels to p53 concentration and distribution.

Purpose of the Study:

  • To investigate the role of p53 in embryonic development arrest induced by oxidative stress during in vitro mammalian embryo culture.
  • To elucidate the molecular pathways through which ROS affects early embryonic development via p53.

Main Methods:

  • Mammalian embryos were exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
  • N-acetyl-L-cysteine (NAC) was used to counteract oxidative stress.
  • The expression of p53, p53-ser15, GADD45a, p21, and cdc2 was analyzed at mRNA and protein levels.
  • Pifithrin-α (PFT-α), a p53 inhibitor, was employed to confirm p53's role.

Main Results:

  • Hydrogen peroxide (H2O2) significantly increased embryo arrest at the two-to-four-cell stage.
  • N-acetyl-L-cysteine (NAC) supplementation reduced embryo arrest, correlating with increased ROS levels.
  • H2O2 treatment elevated p53 and p53-ser15 mRNA and protein levels, alongside increased transcription of p53 targets GADD45a and p21, while reducing cdc2 expression.
  • Inhibition of p53 using PFT-α downregulated GADD45a and p21, upregulated cdc2, and decreased p53 and p53-ser15 protein levels.

Conclusions:

  • Reactive oxygen species (ROS) activate the tumor suppressor p53 pathway during early mammalian embryo development in vitro.
  • Activated p53, through its downstream targets like GADD45a and p21, influences cell cycle progression and contributes to developmental arrest under oxidative stress.
  • Understanding this ROS-p53 axis is crucial for improving in vitro embryo culture conditions and addressing developmental anomalies.
Keywords:
De-Bao Hu and Zhong-Shu Li contributed equally to this study.Early mouse embryo in vitro cultureMouseOxidative stressP53

More Related Videos

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells10:00

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells

Published on: December 11, 2020

3.0K
Visualizing the Effects of Oxidative Damage on Drosophila Egg Chambers using Live Imaging09:20

Visualizing the Effects of Oxidative Damage on Drosophila Egg Chambers using Live Imaging

Published on: April 10, 2021

4.2K

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
10.3K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.3K