Doctoral thesis projects
Find a doctoral thesis project without an attached scholarship. We strongly encourage you to seek other funding sources, including Massey-wide scholarships.
Vascular endothelial growth factor C and VEGFR3 in heart disease patients
Vascular endothelial growth factor C and VEGFR3 in heart disease patients Investigations of vascular endothelial growth factor C (VEGF-C), soluble VEGFR3 levels and VEGF system genetic variation in heart disease cohort samples.
| Closing date | Subject area | Location | Contact |
|---|---|---|---|
| No closing date | Health sciences | Wellington campus | Dr Barry Palmer |
Preferred candidate
A PhD candidate with a background in biochemistry and/or molecular biology who wants to undertake research in the field of assessing heart disease biomarkers.
Eligibility
To be eligible, you need to:
- have a master’s or bachelor’s degree with honours (or equivalent) in a relevant discipline
- know about the assaying of protein markers from plasma and/or the analysis of genetic polymorphisms
- be enthusiastic for challenges
- be well-organised, self-motivated and keen to learn new skills and knowledge.
Experience in ELISA assays and real-time qPCR assays would be advantageous, but is not essential.
To be eligible for a Massey University Doctoral Scholarship, a minimum New Zealand GPA of 7.5 is required (approximately A- average) or a minimum GPA of 3.33 on the United States scale.
About this project
This project is an extension of investigation into baseline levels of components of the vascular endothelial growth factor (VEGF) system (a proxy for angiogenic potential) in heart disease patient plasma and DNA samples.
VEGF-C binds VEGFR2 (KDR) and VEGFR3 (FLT4 — fms-like tyrosine kinase 4) and regulates growth of vessels in the lymphatic system. As well as its role in lymphangiogenesis, VEGF-C’s interaction with VEGFR2 may lead to angiogenesis by regulating a specialised subset of endothelial cells that express VEGFR2.
VEGF-C also induces the activation of VEGFR3+ dendritic cells — stimulating their migration and maturation, potentially influencing immune and inflammatory responses to coronary heart disease. Soluble VEGFR3 (sVEGFR3) has been proposed as an angiogenic biomarker in cancer diagnosis and treatment, and may have use as a prognostic biomarker in heart patients.
Lymphangiogenesis has been observed in humans after heart attack. VEGF-C mRNA expression has been shown to be upregulated in heart biopsies from heart failure patients with either ischaemic (ICM) or dilated cardiomyopathy (DCM) compared to samples from donated, non-failing hearts.
In mice, myocardial ischaemia or ischaemia-reperfusion leads to VEGF-C and VEGFR3 protein over-expression. VEGFR3 blockade and treatment with VEGF-C neutralising antibody reduces the boost in lymphatic vessel density, blunts lymphatic transport, increases inflammation, increases oedema, and increases cardiac dysfunction.
Stimulating the endogenous lymphangiogenesis response with VEGF-C treatment reduces inflammation, reduces oedema, and improves cardiac dysfunction. High levels of VEGF-C in human circulation may positively affect recovery from acute heart disease events.
How to apply
Email Dr Barry Palmer: B.Palmer@massey.ac.nz.
Please send the following documents with your enquiry email:
- cover letter
- CV with referees
- academic record.