OxTalks will soon move to the new Halo platform and will become 'Oxford Events.' There will be a need for an OxTalks freeze. This was previously planned for Friday 14th November – a new date will be shared as soon as it is available (full details will be available on the Staff Gateway).
In the meantime, the OxTalks site will remain active and events will continue to be published.
If staff have any questions about the Oxford Events launch, please contact halo@digital.ox.ac.uk
Mitochondrial function is critical to trophoblast survival and placental homeostasis. Mitochondria are classically thought of as ‘the powerhouses’ of the cell but they also play important roles in metabolism, steroidogenesis and cell signalling. They also must adapt to cell stress and constantly undergo transformation through cycles of fusion and fission.
Recently, we have examined the adaptions and transformations that are evident in mitochondria from late on-set preeclamptic placental tissue compared to early onset (<30 weeks) and normal term tissue. We have examined mitochondrial bioenergetics, dynamics and cell signalling using a variety of cellular and molecular methods and will present data that indicates that mitochondrial adaptions and survival are critical in prolonging placental function during preeclampsia.
Additionally, we have used differential centrifugation to isolate morphologically distinct populations of mitochondria from cytotrophoblast and the syncytium. We will present data on various aspects of their biology including bioenergetics, steroidogenesis and dynamics. We have also conducted a comprehensive proteomic analysis of these isolated mitochondria which has highlighted important switches in cellular metabolism post trophoblast differentiation and fusion.
Finally, we will present evidence on the importance of selenoproteins at the mitochondrial/ER interface and suggest that these might play an important role in alleviating oxidative stress. Selenium supplementation may provide a simple, applicable intervention to protect mitochondrial/ER from oxidative insult and preserve placental function during gestation.