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Contact Details

Phone
+64 3 479 7329
Email
fiona.mcdonald@otago.ac.nz
Position
Professor
Department
Department of Physiology
Qualifications
DPhil(Oxon)
Research summary
Epithelial sodium channel in blood pressure regulation and cancer
Teaching
  • PHSL 233 Epithelial signalling and polarity
  • PHSL 343 Endocytosis in epithelia; trafficking pathways of the epithelial sodium channel; polycystic kidney disease
  • PHSL 473 Kidney control of blood pressure
Memberships
  • Member of Kidney in Health and Disease Research Group
  • New Zealand Association of Scientists
  • NZ Biochemistry and Molecular Biology Society
  • Physiological Society of NZ
  • Dunedin Company of Physiologists

Research

The McDonald laboratory’s focus is on an ion channel, called ENaC, (epithelial sodium channel) that has diverse roles in the body including kidney control of blood pressure, and restraining breast cancer cell proliferation and migration. This channel operates in many tissues and cells of the body, particularly epithelia.

In the kidney ENaC rescues sodium from the urine and allows sodium to re-enter the blood in times of low blood pressure or salt depletion, promoting water retention and an increase in blood pressure. An increased salt load in the body is associated with high blood pressure conditions, and when a gene coding for ENaC is mutated in humans severe high or low blood pressure conditions develop.

We have identified and studied several proteins that associate with the sodium channel and control ENaC function, and hence blood pressure. We apply a wide range of techniques to study the channel: molecular biological methods, cell biological tools to visualise the cellular location of proteins, biochemical methods to detect the interaction of the channel with other proteins, and electrophysiological methods to gain insight into the effects of other proteins on current generated by the sodium channel.

ENaC is expressed in the mammary duct and is thought to assist in defining the components of milk during lactation. Further, ENaC levels appear to be important in breast cancer prognosis, therefore we are investigating how ENaC influences proliferation, migration and invasion in breast cancer cell lines, together with bioinformatic, transcriptome and exome analyses.

Publications

Kilworth, J. N. K., Munro, M. L., & McDonald, F. J. (2023, August). Investigating the functional interaction between the epithelial sodium channel and Ca2+ signalling in breast cancer. Poster session presented at the 17th New Zealand Medical Sciences Congress (MedSci), Queenstown, New Zealand. Conference Contribution - Poster Presentation (not in published proceedings)

Atta Manu, E., Munro, M., Ware, A., & McDonald, F. (2023, August). The mechanisms through which ENaC negatively modulates breast cancer proliferation and metastasis. Poster session presented at the 17th New Zealand Medical Sciences Congress (MedSci), Queenstown, New Zealand. Conference Contribution - Poster Presentation (not in published proceedings)

Logue, M. J. E., Devor, D. C., McDonald, F. J., & Hamilton, K. L. (2023, August). Retromer- and retriever-associated sorting nexin proteins regulate the trafficking of the Ca2+-activated K+ channel KCa2.3. Verbal presentation at the 17th New Zealand Medical Sciences Congress (MedSci), Queenstown, New Zealand. Conference Contribution - Verbal presentation and other Conference outputs

Kumar, S. S., Bouwer, G. T., Jackson, M. K., Perkinson, M. R., McDonald, F. J., Brown, C. H., & Augustine, R. A. (2023). Kisspeptin neuron projections to oxytocin neurons are not necessary for parturition in the mouse. Brain Structure & Function, 228, 1535-1548. doi: 10.1007/s00429-023-02670-7 Journal - Research Article

Hamilton, K., Logue, M., Chueng, T., Pilmore, E., Devor, D., & McDonald, F. (2023). Retromer involvement in trafficking of the calcium-activated K channel, KCa3.1. Physiology, 38(Suppl. 1). doi: 10.1152/physiol.2023.38.S1.5733913 Conference Contribution - Published proceedings: Abstract

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