Amanda Highet

Dr Amanda Highet

Manager, Research Compliance

Research Services

Research and Innovation

As a researcher in the Placental Development Laboratory my work focuses on identifying the key regulators of trophoblast cell function and early placental development. 

During normal pregnancy there is extensive structural remodelling of high-resistance spiral arteries of the uterus into low-resistance, high-capacity vessels to permit adequate blood flow to the placenta.  A subpopulation of placental trophoblast cells, the extravillous cytotrophoblasts (EVT), invade these maternal blood vessels where they replace the endothelial lining and degrade most of the musculo-elastic tissue in the vessel walls. The spiral arteries are plugged by invading endovascular EVTs to restrict blood flow and sustain a low oxygen environment of 1-2% oxygen, until the plugs are removed and maternal blood fills the intevillous space. I am investigating how the maintanance of the low oxygen environment promotes trophoblast invasion and differentiation early in the first trimester, and how the placenta responds to the oxidative stress associated with the onset of maternal blood flow. 

Date Position Institution name
2021 - ongoing Senior Research Compliance Officer The University of Adelaide
2016 - 2022 Research Compliance Officer (Gene Technology) The University of Adelaide
2011 - 2016 NHMRC Australian Biomedical Training Fellow University of Adelaide

Date Institution name Country Title
2007 - 2009 University of Adelaide Australia PhD
2002 - 2006 University of South Australia Australia Bachelor of Laboratory Medicine

Year Citation
2017 Highet, A., Bianco-Miotto, T., Pringle, K., Peura, A., Bent, S., Zhang, J., . . . Roberts, C. (2017). A novel embryo culture media supplement that improves pregnancy rates in mice. Reproduction, 153(3), 327-340.
DOI Scopus12 WoS11 Europe PMC11
2016 Highet, A., Buckberry, S., Mayne, B., Khoda, S., Bianco-Miotto, T., & Roberts, C. (2016). First trimester trophoblasts forming endothelial-like tubes in vitro emulate a ‘blood vessel development’ gene expression profile. Gene Expression Patterns, 21(2), 103-110.
DOI Scopus18 WoS17 Europe PMC15
2015 Standen, P., Sferruzzi-Perri, A., Taylor, R., Heinemann, G., Zhang, J., Highet, A., . . . Roberts, C. (2015). Maternal insulin-like growth factor 1 and 2 differentially affect the renin-angiotensin system during pregnancy in the guinea pig. Growth Hormone & IGF Research, 25(3), 141-147.
DOI Scopus4 WoS4 Europe PMC4
2015 Highet, A., Khoda, S., Buckberry, S., Leemaqz, S., Bianco-Miotto, T., Harrington, E., . . . Roberts, C. (2015). Hypoxia induced HIF-1/HIF-2 activity alters trophoblast transcriptional regulation and promotes invasion. European Journal of Cell Biology, 94(12), 589-602.
DOI Scopus65 WoS58 Europe PMC53
2014 Highet, A., Berry, A., Bettelheim, K., & Goldwater, P. (2014). Gut microbiome in sudden infant death syndrome (SIDS) differs from that in healthy comparison babies and offers an explanation for the risk factor of prone position. International Journal of Medical Microbiology, 304(5-6), 735-741.
DOI Scopus42 WoS37 Europe PMC32
2013 Highet, A., & Goldwater, P. (2013). Maternal and perinatal risk factors for SIDS: a novel analysis utilizing pregnancy outcome data. European Journal of Pediatrics, 172(3), 369-372.
DOI Scopus8 WoS8 Europe PMC6
2012 Highet, A., Zhang, V., Heinemann, G., & Roberts, C. (2012). Use of Matrigel in culture affects cell phenotype and gene expression in the first trimester trophoblast cell line HTR8/SVneo. Placenta, 33(7), 586-588.
DOI Scopus29 WoS29 Europe PMC24
2011 McMichael, G., Highet, A., Gibson, C., Goldwater, P., O'Callaghan, M., Alvino, E., & MacLennan, A. (2011). Comparison of DNA extraction methods from small samples of newborn screening cards suitable for retrospective perinatal viral research. Journal of Biomolecular Techniques, 22(1), 5-9.
Scopus8 Europe PMC4
2011 Highet, A., Gibson, C., & Goldwater, P. (2011). CD14 (C-260T) polymorphism is not associated with sudden infant death syndrome (SIDS) in a large South Australian cohort. Innate Immunity, 17(3), 321-326.
DOI Scopus3 WoS3 Europe PMC3
2010 Highet, A., Gibson, C., & Goldwater, P. (2010). Variant interleukin 1 receptor antagonist gene alleles in sudden infant death syndrome. Archives of Disease in Childhood, 95(12), 1009-1012.
DOI Scopus9 WoS8 Europe PMC7
2010 Highet, A., Berry, A., & Goldwater, P. (2010). Distribution of interleukin-1 receptor antagonist genotypes in Sudden Unexpected Death in Infancy (SUDI); unexplained SUDI have a higher frequency of allele 2. Annals of Medicine, 42(1), 64-69.
DOI Scopus12 WoS9 Europe PMC8
2010 Highet, A., Gibson, C., & Goldwater, P. (2010). A polymorphism in a staphylococcal enterotoxin receptor gene (T cell receptor BV3 recombination signal sequence) is not associated with unexplained sudden unexpected death in infancy in an Australian cohort. Microbial Pathogenesis, 49(1-2), 51-53.
DOI Scopus1 WoS1 Europe PMC1
2010 Highet, A., Gibson, C., & Goldwater, P. (2010). Clostridium sordellii lethal toxin gene is not detectable by PCR in the intestinal flora of infants who died from sudden infant death syndrome or other causes. Journal of Medical Microbiology, 59(2), 251-253.
DOI Scopus2 WoS2 Europe PMC2
2009 Highet, A., Berry, A., & Goldwater, P. (2009). Novel hypothesis for unexplained sudden unexpected death in infancy (SUDI). Archives of Disease in Childhood, 94(11), 841-843.
DOI Scopus15 WoS13 Europe PMC9
2009 Highet, A., & Goldwater, P. (2009). Staphylococcal enterotoxin genes are common in Staphylococcus aureus intestinal flora in Sudden Infant Death Syndrome (SIDS) and live comparison infants. FEMS Immunology and Medical Microbiology, 57(2), 151-155.
DOI Scopus25 WoS25 Europe PMC23
2009 Highet, A., Berry, A., Bettelheim, K., & Goldwater, P. (2009). The frequency of molecular detection of virulence genes encoding cytolysin A, high-pathogenicity island and cytolethal distending toxin of Escherichia coli in cases of sudden infant death syndrome does not differ from that in other infant deaths and healthy infants. Journal of Medical Microbiology, 58(3), 285-289.
DOI Scopus14 WoS13 Europe PMC10
2008 Highet, A. (2008). An infectious aetiology of sudden infant death syndrome. Journal of Applied Microbiology, 105(3), 625-635.
DOI Scopus49 WoS41 Europe PMC37

2011-2017 (part time from 2014) NHMRC Australian Biomedical Training Fellowship $290,032. Project title: Essential stages in the early development of the placenta and their role in preeclampsia

2016 Robinson Research Institute Travel Grant $550. To present at the Society for Reproductive Biology Conference, August 2016, Gold Coast, Australia

2015 Llewellin and Margaret Davey Travel/Skills Competency Award $2230. To present at the International Federation of Placenta Associations (IFPA) conference, September 2015, Brisbane, Australia

2012 Robinson Institute/School of Paediatrics and Reproductive Health Travel Grant $750. To present at Society for Reproductive Biology Conference                                  

2011 Research Centre for Reproductive Health Travel Grant $500. To present at ANZPRA Satellite Meeting and the Society for Reproductive Biology Conference, and to attend the World Congress for Reproductive Biology, Cairns Australia

2007-2009 Foundation for the Study of Infant Deaths (UK) project funding $150,000. The role of novel toxins in the sudden infant death syndrome

2007-2009 Australian Postgraduate Award PhD Scholarship $20,427 pa. Bacterial Toxins and Genetic Variations in the Sudden Infant Death Syndrome

2006 MS McLeod Departmental Research Fund $10,000. Bacterial toxins in Sudden Infant Death Syndrome

Research Project in Reproductive Health Tutorial- Presenting research results –figures, tables and text

Date Role Research Topic Program Degree Type Student Load Student Name
2013 - 2015 Co-Supervisor Hypoxia Induced HIF-1/HIF-2 Activity alters Trophoblast Transcriptional Regulation across Gestation Master of Philosophy (Medical Science) Master Full Time Mrs Sultana Mahabbat-e Khoda

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