Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
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.