Dr Katja Rietdorf

Professional biography

I am a cell physiologist specialising in calcium signalling and the regulation of calcium channels. My PhD was obtained in the laboratory of Bernd Walz at the University of Potsdam in Germany on the topic of ‘Signalling Pathways that Stimulate Protein and Fluid Secretion in Cockroach Salivary Glands’. This was followed by studying IP₃ receptor-interacting proteins in Martin Bootman and Mike Berridge’s laboratory at The Babraham Institute in Cambridge, and the characterisation of two-pore channels (TPCs) as endolysosomal calcium channels activated by the second messenger NAADP in Antony Galione’s laboratory at Oxford University. Subsequently I joined the laboratory of Michael Sanderson at UMASS Medical School in Worcester, MA, USA and started working on a special type of cardiac cells called pulmonary vein sleeve cells (PVCs). From UMASS I moved to The Open University, first as a Research Fellow, before I became a Lecturer in Biology in 2016 and a Senior Lecturer in 2021.

Research interests

My research focusses on the role of calcium signalling in health and disease, especially in cardiac cells and cancer. Much of my work has focussed on the regulation of intracellular calcium release channels, namely IP₃ receptors and ryanodine receptors localised on the endo- or sarcoplasmic reticulum, and two-pore channels (TPCs) on endosomes and lysosomes. 

Over the past years, we have worked on a pro-arrhythmic type of cardiac myocyte that is located in the pulmonary vein, called pulmonary vein sleeve cells (PVCs). The spontaneous activity of these cells is one of the main causes of atrial fibrillation, the most common form of cardiac arrhythmia. In one of our projects, we are characterising the structural and functional changes that occur in PVCs during ageing.

Based on my interest in endolysosomal ion channels, especially TPCs, and the fact that recent work provided evidence that the activity of TPCs can modulate the function of cardiac myocytes, we are studying how lysosomal ion channels contribute to the function of healthy cardiac myocytes. Individuals with the lysosomal storage disorder CLN3 (also called juvenile dementia) develop cardiac dysfunction during their disease progression. CLN3 belongs to a group of lysosomal storage disorders called Neuronal Ceroid Lipofuscinoses (NCLs). To study what causes the decline in the cardiac function observed in CLN3 patients, we are comparing the structure and function of iPSC-derived cardiac myocytes using cells from patients with and without mutations in the CLN3 gene.

In other projects in the laboratory study the role of calcium in cancer and autophagy. A current PhD student studies the roleof calcium-signalling genes in the progression of prostate cancer to neuroendocrine prostante cancer (NEPC). 

Teaching interests

MRP Chair and module team co-chair for S296: Cell and molecular biology

Module team member for S317: Biological science: From genes to species 

External collaborations

Dr Katharine Dibb, Manchester University (Studying the structure and function of PVCs)