Mechanisms behind fetal vascular dysfunction in diabetic pregnancies
Fact file
| Duration |
Three to four years full-time |
|---|
| Eligibility |
Self-funded; Home, EU or International Students |
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| Supervisor(s) |
Lopa Leach |
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| Application deadline |
No deadline |
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About the project
The central research focus of our group is to understand the mechanisms regulating two key functions of human blood vessels: permeability and angiogenesis. We are specifically interested in the role of junctional adhesion molecules and how their impairment can lead to placental and fetal vascular dysfunction in pregnancies complicated by diabetes mellitus. We use the extra-corporeally perfused term placenta and isolated human endothelial cells as complementary experimental models. This allows a powerful integration of physiology, confocal imaging and molecular biology. We also have a human in vitro model of the outer-retinal barrier which allows studies into neo-vascularisation, a complication of age-related macula degeneration.
This project will be looking at transmigration behaviour of stem cells acquired from the human placenta and cord and how they affect endothelial barrier function.
Funding notes
This project is available to self-funded students. Home applicants should contact the supervisor to determine the current funding status for this project. EU applicants should visit the Graduate School webpages for information on specific EU scholarships. International applicants should visit our International Research Scholarships page for information regarding fees and funding at the University.
See this project on FindaPhD
Mechanisms behind fetal vascular dysfunction in diabetic pregnancies