John Philip Winpenny

Physiology; Medical education; Widening access; Assessment; Ion channels

John gained a BSc (Hons) (Anatomy & Physiology, University of Dundee), PhD (Anatomy & Physiology, University of Dundee), and a PGCert Higher Education Practice (University of East Anglia).

John is a full member of the Physiological Society of Great Britain, a regular member of the American Physiological Society and a Fellow of the Higher Education Academy (FHEA).

John is a Senior Lecturer in Physiology and Director of Inclusion in the School of Medicine, University of St Andrews.

After graduating with a BSc in Physiology (1988) from Dundee University, John completed a PhD (1992) at Dundee University on the effects of simple anaesthethic molecules and potassium ion channels in snail neurons.  He moved to Newcastle University to investigate the secretion of bicarbonate in pancreatic ducts and the chloride ion channel responsible for cystic fibrosis (1992-1996). During this period, he successful applied for his own Wellcome Trust Fellowship, which allowed him to work in the USA (1996-1999), before returning to a first lectureship position at Sunderland Pharmacy School (1999-2004). He moved to a lectureship (then promotion to senior lecturer) at the then new Medical School at the University of East Anglia (2004-2020), before returning (in 2020) to Scotland and to the School of Medicine at St Andrews.

John has a very active role in teaching and management within the School of Medicine. John is the Year 2 lead for the Scottish Graduate Entry Medicine (ScotGEM) programme. He teaches Physiology throughout the currciulum of both the BSC Medicine and ScotGEM programmes. He is a personal adviser to BSc Medicine (Years 1-3) and ScotGEM MBChB students (Years 1-2). He is also a Portfolio Supervisor to ScotGEM students (Years 1-4).

He has been an External Examiner at several Institutions (including the Universities of Anglia Ruskin, Southampton, St Georges, Newcastle and Leeds).

Structure-function relationships of ion channels in normal and disease states.

I have investigated the distribution, function and regulation of chloride ion channels. This research has examined both normal and diseased tissues and in particular the function and regulation of chloride ion channels in the disease cystic fibrosis (CF). CF is an autosomal recessive genetic disease that is caused by mutations in the CF gene encoding the CFTR chloride channel. These mutations result in defective trafficking and/or regulation of the apical CFTR chloride channel. In the airways, defective CFTR leads to impaired mucociliary clearance, abnormally thick mucous secretions, chronic bacterial infections and inflammation of the lung. In the pancreas, defective CFTR leads to blockage of the duct cells and eventual fibrosis of the gland. Several potential strategies have been investigated as possible therapies for CF, including targeted gene therapy, and pharmacological approaches that aim to activate the CFTR channel.

My interest has been in another approach, which involves activation of alternative chloride ion channels present in CF cells. Calcium-activated chloride (CaC) channels are one such protein that are found in many secretory epithelia. Strong evidence supporting this alternative ion channel approach is provide by results from transgenic CF knockout mice in which organs exhibiting little or no pathology all have a significant CaC conductance. Organs with no CaC conductance show significant pathology. The cloning of several putative calcium-sensitive chloride channel proteins from mouse and human tissues have been reported, including the CLCA, bestrophin and anoctamin gene families.

Educational Research: