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Published on: May 17, 2024
A differential autophagic response to hyperglycemia in the developing murine embryo
Katie L Adastra1, Maggie M Chi, Joan K Riley
1Department of Obstetrics and Gynecology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8064, Saint Louis, Missouri 63110, USA.
Abstract:
Autophagy is critical to the process of development because mouse models have shown that lack of autophagy leads to developmental arrest during the pre-implantation stage of embryogenesis. The process of autophagy is regulated through signaling pathways, which respond to the cellular environment. Therefore, any alteration in the environment may lead to the dysregulation of the autophagic process potentially resulting in cell death. Using both in vitro and in vivo models to study autophagy in the pre-implantation murine embryo, we observed that the cells respond to environmental stressors (i.e. hyperglycemic environment) by increasing activation of autophagy in a differential pattern within the embryo. This upregulation is accompanied by an increase in apoptosis, which appears to plateau at high concentrations of glucose. The activation of the autophagic pathway was further confirmed by an increase in GAPDH activity in both in vivo and in vitro hyperglycemic models, which has been linked to autophagy through the activation of the Atg12 gene. Furthermore, this increase in autophagy in response to a hyperglycemic environment was observed as early as the oocyte stage. In conclusion, in this study, we provided evidence for a differential response of elevated activation of autophagy in embryos and oocytes exposed to a hyperglycemic environment.
Insights
Autophagy, a key cellular process, is upregulated in mouse embryos and oocytes exposed to high glucose. This response, involving increased apoptosis, highlights the impact of environmental factors on early development.
Area of Science:
- Cell Biology
- Developmental Biology
- Reproductive Science
Background:
- Autophagy is essential for embryonic development, with its absence causing developmental arrest.
- Cellular signaling pathways regulate autophagy in response to environmental cues.
- Environmental alterations can disrupt autophagy, potentially leading to cell death.
Purpose of the Study:
- To investigate the role of autophagy in pre-implantation embryos under hyperglycemic conditions.
- To examine the cellular response to environmental stressors during early embryogenesis.
- To determine if autophagy is activated in oocytes and embryos exposed to high glucose.
Main Methods:
- Utilized in vitro and in vivo murine models.
- Exposed embryos and oocytes to hyperglycemic environments.
- Measured autophagy activation and apoptosis levels.
- Assessed Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and Atg12 gene expression.
Main Results:
- Embryos and oocytes showed increased autophagy activation in response to a hyperglycemic environment.
- Autophagy activation occurred in a differential pattern within the embryo.
- Increased apoptosis was observed, plateauing at high glucose concentrations.
- GAPDH activity and Atg12 gene expression confirmed autophagic pathway activation.
Conclusions:
- Hyperglycemia induces a differential activation of autophagy in pre-implantation embryos.
- Oocytes also exhibit elevated autophagy in response to high glucose.
- Autophagy plays a significant role in the cellular response to metabolic stress during early development.
