Related Experiment Video
Updated: Aug 2, 2025
06:53
Vitrification of In Vitro Matured Oocytes Collected from Adult and Prepubertal Ovaries in Sheep
Published on: July 10, 2021
5.2K
Ru360 protects against vitrification-induced oocyte meiotic defects by restoring mitochondrial function
Haowei Sun1, Yaoyao Guo1, Ruochun Yu1
1Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Theriogenology
|April 14, 2023
Summary
Oocyte vitrification can harm immature egg cell maturation, causing aneuploidy. Inhibiting mitochondrial calcium influx can restore function and prevent these defects, improving fertility preservation.
Area of Science:
- Reproductive biology
- Cell biology
- Cryobiology
Background:
- Oocyte vitrification is a key technique for female fertility preservation.
- Vitrification of immature (germinal vesicle stage, GV) oocytes is linked to increased aneuploidy risk during meiotic maturation.
- The mechanisms and preventative strategies for these vitrification-induced defects are not well understood.
Purpose of the Study:
- To investigate the molecular mechanisms underlying meiotic maturation defects in vitrified GV oocytes.
- To identify potential strategies to mitigate these adverse effects and improve oocyte cryopreservation outcomes.
Main Methods:
- Comparison of first polar body extrusion rates and aneuploidy rates between vitrified and non-vitrified GV oocytes.
- Assessment of meiotic maturation defects, including spindle morphology, chromosome alignment, Kinetochore-Microtubule (KT-MT) attachments, and spindle assembly checkpoint (SAC) protein complex function.
- Analysis of mitochondrial function, specifically mitochondrial calcium (Ca2+) levels.
- Evaluation of the effect of inhibiting mitochondrial Ca2+ entry using Ru360 on meiotic defects.
Main Results:
- Vitrification of GV oocytes significantly decreased the first polar body extrusion rate and increased the aneuploidy rate.
- Defects observed included aberrant spindle morphology, chromosome misalignment, incorrect KT-MT attachments, and weakened SAC function.
- Vitrification disrupted mitochondrial function by increasing mitochondrial Ca2+ levels.
- Inhibition of mitochondrial Ca2+ entry with Ru360 restored mitochondrial function and rescued meiotic defects.
Conclusions:
- Increased mitochondrial Ca2+ is a significant cause of meiotic defects in vitrified GV oocytes.
- These findings elucidate the molecular mechanisms of oocyte vitrification-induced adverse effects on meiotic maturation.
- Targeting mitochondrial Ca2+ offers a potential strategy to enhance oocyte cryopreservation protocols.
