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Melatonin Promotes in vitro Development of Vitrified-Warmed Mouse GV Oocytes, Potentially by Modulating
Jianpeng Qin1, Shichao Guo1, Jinyu Yang1
1Department of Animal Science, Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, College of Animal Science and Technology, Sichuan Agricultural University, Chengdu, China.
Abstract:
Previous studies have shown that melatonin can mitigate cryopreservation-induced mitochondrial dysfunction in oocytes; however, the underlying molecular mechanism remains unclear. The objective of the present study was to investigate whether melatonin can improve the mitochondrial function during in vitro maturation of vitrified-warmed mouse germinal vesicle (GV) oocytes by modulating phosphorylation of dynamin related protein 1 (Drp1). Vitrification/warming procedures resulted in the following: (1) After cryopreservation of mouse GV oocytes, the phosphorylation level of Drp1 at Ser616 (p-Drp1 Ser616) in metaphase II (MII) oocytes was increased (P < 0.05). Furthermore, the rates of in vitro maturation, cleavage and blastocyst formation after parthenogenetic activation were decreased (P < 0.05). (2) In MII oocytes, the expression levels of translocase of the mitochondrial outer membrane 20 (TOMM20), mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) content, and mRNA levels of mitochondrial biogenesis-related genes (Sirt1, Pgc-1α, Tfam) were all decreased (P < 0.05), and (3) Reactive oxygen species (ROS) level, early apoptosis level, Cytochrome C release and mRNA levels of pro-apoptotic related genes (Bax, Caspase9, Caspase3) in MII oocytes were all increased (P < 0.05). The results of this study further revealed that negative impacts of GV oocyte cryopreservation were mitigated by supplementation of warming and in vitro maturation media with 10-7mol /L melatonin or 2 x 10-5mol/L Mdivi-1 (Drp1 inhibitor). Therefore, we concluded that 10-7mol/L melatonin improved mitochondrial function, reduced oxidative stress and inhibited apoptosis by regulating phosphorylation of Drp1, thereby enhancing in vitro development of vitrified-warmed mouse GV oocytes.
Insights
Melatonin protects mouse oocytes from cryopreservation damage by improving mitochondrial function and reducing apoptosis. This study reveals melatonin regulates dynamin related protein 1 (Drp1) phosphorylation, enhancing oocyte development after warming.
Area of Science:
- Reproductive Biology
- Mitochondrial Biology
- Cryobiology
Background:
- Cryopreservation of oocytes can lead to mitochondrial dysfunction, impacting developmental potential.
- The molecular mechanisms by which melatonin mitigates these effects are not fully understood.
Purpose of the Study:
- To investigate if melatonin improves mitochondrial function in vitrified-warmed mouse germinal vesicle (GV) oocytes during in vitro maturation.
- To determine if melatonin modulates the phosphorylation of dynamin related protein 1 (Drp1) to achieve these effects.
Main Methods:
- Vitrification and warming of mouse GV oocytes.
- Assessment of Drp1 phosphorylation (p-Drp1 Ser616) in metaphase II (MII) oocytes.
- Evaluation of mitochondrial parameters (TOMM20, MMP, ATP), oxidative stress (ROS), apoptosis markers, and developmental rates.
- Treatment with melatonin or a Drp1 inhibitor (Mdivi-1).
Main Results:
- Cryopreservation increased p-Drp1 Ser616, decreased mitochondrial function markers and developmental rates, while increasing ROS and apoptosis.
- Melatonin (10⁻⁷ mol/L) and Mdivi-1 (2 x 10⁻⁵ mol/L) mitigated the negative impacts of cryopreservation.
- Melatonin treatment improved mitochondrial function, reduced oxidative stress and apoptosis in vitrified-warmed oocytes.
Conclusions:
- Melatonin enhances the in vitro development of vitrified-warmed mouse GV oocytes.
- Melatonin exerts its protective effects by regulating Drp1 phosphorylation, thereby improving mitochondrial function and reducing cellular stress.
