Hellgren 2017 MiPschool Obergurgl
Event: MiPschool Obergurgl 2017
Prenatal hypoxia can lead to latent phenotypical changes in the adult cardiovascular system, including altered cardiac structure/function and increased susceptibility to ischemia reperfusion injury. While the cellular mechanisms underlying this phenomenon are largely unknown, several studies have pointed towards cardiac metabolic disturbances in the offspring of hypoxic pregnancies. We investigated mitochondrial function in the offspring from a mouse model of prenatal hypoxia. Pregnant C57 mice were subjected to either normoxia (21%) or hypoxia (14%) during gestational days 6-18. Offspring were reared in normoxia for 6 months and mitochondrial function was assessed in cardiac homogenates using a substrate-uncoupler-inhibitor (SUIT) protocol with an Oroboros O2k coupled with the O2k-Fluo LED2-module.
Our data show that female adult offspring from hypoxic pregnancies have an increased aerobic capacity and a reduced ROS production, compared to their normoxic counterparts. This was in contrast to males from hypoxic pregnancies that showed no changes in respiration and a trend towards increased ROS production.
Preliminary results suggest the mechanism behind the altered respiration in females may involve complex I or relate to differences in ROS production and/or antioxidant capacity. These mechanisms are currently under investigation, but our results clearly show prenatal hypoxia can have long-lasting effects on cardiac metabolism. Therefore, our study has important implications for the management of cardiac disease in patients from complicated pregnancies.
Labels: MiParea: Respiration
Stress:Hypoxia Organism: Mouse Tissue;cell: Heart Preparation: Homogenate
Coupling state: LEAK, ROUTINE, ET Pathway: N HRR: Oxygraph-2k, O2k-Fluorometer Event: A1, Oral
Affiliations and support
- Div Cardiovasc Siences, Univ Manchester, United Kingdom. – email@example.com
Selected mentor: Dr. Gina Galli