Staff profile - Kathryn Aston-Mourney

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Dr Kathryn Aston-Mourney

Position: Lecturer in Human Biology
Faculty or Division: Faculty of Health
Department: School of Medicine
Campus: Geelong Waurn Ponds Campus
Phone: +61 3 52272977 +61 3 52272977
Email: k.astonmourney@deakin.edu.au

Biography

Qualifications

  • Doctor of Philosophy, University of Melbourne, 2007


Academic

Subjects and units currently teaching

Post-graduate Medicine

HME101: Medicine 1A Unit Coordinator

Human Biology Topic Coordinator

 

Under-graduate Medical Biotechnology

HMM103: Cell Technology Unit Chair


Student supervision

- Development of a Beta-cell Gene Expression Signature to Identify New Drugs for the Treatement of Diabetes

- HDAC Inhibition as a Potential Therapy for Preventing the Progression of Type 2 Diabetes

- Beta-cell Regeneration Using the Zebrafish Model

- The Role of Copper in Beta-cell Function


Awards

Awards and prizes

2012 JDRF/Maquarie Group Foundation Early-Stage Researcher Travel Grant
2012 CASS Foundation Early Career Researcher Award
2009 Travel Scholarship, Recent Advances in Beta Cell Biology, International Diabetes Federation and University of Toronto
2006 Travel Scholarship, Australian Diabetes Society
2005 Pincus-Taft Young Investigator Award (Awarded by the Australian Diabetes Society)
2005 Travel Scholarship, Australian Diabetes Society
2005  Sanofi aventis Diabetes Partnership Young Investigator Award:   Travel Grant for American Diabetes Association Annual Scientific Meeting 2005
2004 Travel Scholarship, Australian Diabetes Society
2003-2007 Australian Postgraduate Award (Scholarship)
2003 Travel Scholarship, Australian Diabetes Society


Research

Research projects

Dr. Aston-Mourney has several projects underway focusing on the insulin-secreting beta cells of the pancreas and their dysfunction in diabetes.

 

Currently accepting expressions of interest from prospective PhD and Honours students.


Research grants

2015     Geelong Community Foundation (Sole CI) - $32,000
Discovery of Novel Therapies for Type 2 Diabetes

2015     Sir Edward Dunlop Medical Research Foundation Research Grant (Sole CI) - $20,000
Generation and Application of a Novel Screening Tool for the Discovery of β-cell Protective Diabetes Drugs

2015     CASS Foundation Medical Project Grant (CIA) - $55,000
HDAC Inhibition as a Potential Therapy for Preventing the Progression of Type 2 Diabetes.

2014     Deakin University Central Research Grants Scheme (Sole CI) - $28,500
Discovery of Novel Drugs for Type 2 Dabetes

2013     Deakin University Research Equipment Support Scheme  (CIA) - $120,000
For purchase of Next Generation Sequencing equipment

2012   CASS Foundation Early Career Researcher Award  (Sole CI) - $3000
For travel to the American Diabetes Association 72nd Scientific Sessions, Philadelphia, PA, USA

2012    JDRF/Maquarie Group Foundation Early-Stage Researcher Grant  (Sole CI) - $3170
For travel to the Keystone Islet Biology Symposium, Monterey, CA, USA

07/25/2011 – 07/25/2013  Alfred Deakin Fellowship     (Sole CI) - $180,000
Molecular and Medical Research Strategic Research Centre, Deakin University.
Using Beta-cell Gene Expression Signature to Identify Mechanisms of Beta-cell Dysfunction and Restoration of Function

08/01/2009 – 07/25/2011 McAbee Fellowship (Sole CI) - $109,000
Diabetes and Endocrinology Research Centre, University of Washington.
The role of matrix metalloproteinase-9 to limit islet amyloid deposition in diabetes.

2005 Sanofi Aventis Diabetes Partnership Young Investigator Award (Sole CI) - $3000
For travel to the American Diabetes Association 65th Scientific Sessions, San Diego, CA, USA


Publications

Publications

Aston-Mourney K, et al. “One year of sitagliptin treatment protects against islet amyloid-associated beta-cell loss and does not induce pancreatitis or pancreatic neoplasia in mice”, Am J Physiol Endocrinol Metab. 2013. 

Smits MM, Woudstra P, et al.“Adipocytokines as features of the metabolic syndrome determined using confirmatory factor analysis”, Ann Epidemiol. 2013.

Udayasankar J, Zraika S, et al. “Rosiglitazone treatment does not decrease amyloid deposition in transplanted islets from transgenic mice expressing human islet amyloid polypeptide”, Transplant Proc. 2013.

Aston-Mourney K, Zraika S, et al. “Matrix metalloproteinase-9 reduces islet amyloid formation by degrading islet amyloid polypeptide.” J Biol Chem. 2013.

Subramanian SL, Hull RL, et al. “cJUN N-terminal kinase (JNK) activation mediates islet amyloid-induced beta cell apoptosis in cultured human islet amyloid polypeptide transgenic mouse islets.” Diabetologia. 2012.

Jurgens CA, Toukatly MN, et al. “β-cell loss and β-cell apoptosis in human type 2 diabetes are related to islet amyloid deposition” Am J Pathol. 2011.

Aston-Mourney K, Hull RL, et al. “Exendin-4 increases islet amyloid deposition but offsets the resultant beta cell toxicity in human islet amyloid polypeptide transgenic mouse islets.” Diabetologia. 2011.

Zraika S, Aston-Mourney K, et al. “Neprilysin impedes islet amyloid formation by inhibition of fibril formation rather than peptide degradation.”  J Biol Chem. 2010.

Hull RL, Zraika S, et al. “Amyloid formation in human IAPP transgenic mouse islets and pancreas, and human pancreas, is not associated with endoplasmic reticulum stress.” Diabetologia. 2009.

Zraika S, Hull RL, et al. “Oxidative stress is induced by islet amyloid formation and time-dependently mediates amyloid-induced beta cell apoptosis.” Diabetologia. 2009.

Udayasankar J, Kodama K, et al. “Amyloid formation results in recurrence of hyperglycaemia following transplantation of human IAPP transgenic mouse islets” Diabetologia. 2009.

Kebede M, Favaloro J, et al. “Fructose-1,6-bisphosphatase overexpression in pancreatic beta-cells results in reduced insulin secretion: a new mechanism for fat-induced impairment of beta-cell function” Diabetes. 2008.

Aston-Mourney K, Proietto J, et al. “Too much of a good thing: why it is bad to stimulate the beta cell to secrete insulin” Diabetologia. 2008.

Aston-Mourney K, Wong N, et al. “Increased nicotinamide nucleotide transhydrogenase levels predispose to insulin hypersecretion in a mouse strain susceptible to diabetes.” Diabetologia. 2007.

Zraika S, Aston-Mourney K, et al. “The influence of genetic background on the induction of oxidative stress and impaired insulin secretion in mouse islets.”  Diabetologia. 2006.

Andrikopoulos S, Massa CM, et al. “Differential effect of inbred mouse strain (C57BL/6, DBA/2, 129T2) on insulin secretory function in response to a high fat diet.” J Endocrinol. 2005.

Aston-Mourney K, Proietto J, Andrikopoulos S. “Investigational agents that protect pancreatic islet beta-cells from failure.” Expert Opin Investig Drugs. 2005.

Kooptiwut S, Kebede M, et al. “High glucose-induced impairment in insulin secretion is associated with reduction in islet glucokinase in a mouse model of susceptibility to islet dysfunction.” J Mol Endocrinol. 2005.


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