Elucidating the role of SPINT1 in placental insufficiency
- Research Opportunity
- Obstetrics and Gynaecology
- Austin Health
|Associate Professor Tu'uhevaha Kaitu'u-Linofirstname.lastname@example.org||8458 4355||Personal web page|
|Associate Professor Natalie Hannanemail@example.com||Personal web page|
Summary Poor placental function can result in fetal growth restriction and ultimately stillbirth. We have recently identified SPINT1 as a protein dysregulated in women carrying a small baby. The aim of this project will be to elucidate the regulatory mechanisms of SPINT1 in placental function using animal models and samples collected from women delivering at the Mercy Hospital for Women.
Good placental function is essential to a successful pregnancy. Placental insufficiency is when placental function is poor and it can result in serious pregnancy complications such as preeclampsia and fetal growth restriction. It is now well established that fetal growth restriction is a leading cause of stillbirth; a tragedy that occurs at a rate of 1:130 pregnancies in Australia. Our team have been dedicated to identifying novel blood biomarkers that could predict which babies are poorly grown and thus at risk of stillbirth. Once marker we have identified is a novel placental protein called SPINT1. pp ppPrevious research suggests SPINT1 may be critical to normal placental development in mice, with knockout studies suggesting it is particularly important in the formation of the maternal fetal interface - where blood and nutrient exchange occurs. The aim of this project is to begin to tease out the contribution of SPINT1 to normal placental functions in humans - using primary human cells and tissues. In addition we plan to embark upon elegant mouse studies (placental specific knockdown) to really pinpoint the exact time at which SPINT1 becomes critical for normal placental development. p
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