Hellgren 2017 MiPschool Obergurgl

From Bioblast
Jump to: navigation, search
Kim Hellgren IMG 4885.JPG
Effect of prenatal hypoxia on adult mitochondrial respiration and ROS production.

Link: MitoEAGLE

Hellgren KT, Trafford AW, Galli GLJ (2017)

Event: MiPschool Obergurgl 2017

COST Action MitoEAGLE

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.


Bioblast editor: Kandolf G O2k-Network Lab: UK Manchester Galli GL


Labels: MiParea: Respiration 

Stress:Hypoxia  Organism: Mouse  Tissue;cell: Heart  Preparation: Homogenate 


Coupling state: LEAK, ROUTINE, ET  Pathway:HRR: Oxygraph-2k, O2k-Fluorometer  Event: A1, Oral 


Affiliations and support

Div Cardiovasc Siences, Univ Manchester, United Kingdom. – kim.hellgren@postgrad.manchester.ac.uk


Selected mentor: Dr. Gina Galli