QMB Kidney Speakers

Invited speakers

Peter Deen

Peter Deen is Professor of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.

For a proper functioning of epithelial cells, a polarized sorting and localization of channels and transporters that mediate transcellular ion and water movement is essential. One such protein is the aquaporin-2 (AQP2) water channel, whose vasopressin-induced translocation from intracellular vesicles to the apical membrane of the renal collecting duct cells is essential for a proper regulation of pro-urinal water reabsorption and thus our body water homeostasis. My research goals are to increase our understanding of the mechanisms regulating human water homeostasis in health and disease. Nephrogenic Diabetes Insipidus (NDI) is a disease in which the kidney is unresponsive to vasopressin, and can be acquired, as with lithium therapy, or of congenital origin. We discovered that acquired NDI, through lithium, is caused by the influx and elevation to toxic levels of lithium inside the renal principal cells and that blocking the channel mediating this, prevented development of NDI in rats. Congenital NDI is due to mutations in the vasopressin-type 2 receptor (V2R) or AQP2 genes and we found that this usually results in the synthesis of mis-folded, or mis-sorted V2R or AQP2 proteins. As rescuing the mis-sorting/folding of functional AQP2/V2R mutants might relieve patients with NDI, our work also focuses on elucidating the routing regulation of wild-type AQP2/V2R, dissolving the underlying mechanisms for mis-sorting of AQP2 mutants, and the identification of pharmacological chaperones, rescuing the cell surface expression of AQP2/V2R mutants in NDI. Data obtained will be discussed.

H. Moo Kwon

H. Moo Kwon was born and educated in South Korea. He then moved to the United States of America to begin his scientific career. He obtained his PhD in Physiology from the State University of New York followed by post-doctoral training at the National Institutes of Health. He has held faculty positions at Johns Hopkins University and is now at the University of Maryland where he is Professor of Medicine and Physiology.

Professor Kwon discovered the transcription factor, TonEBP (tonicity-responsive enhancer binding protein), which is a central osmoregulatory in the kidney. TonEBP is essential for the urinary concentrating mechanism via its target genes aquaporin 2 (AQP2) and urea (UT-A) transporters. TonEBP is also critical for cellular adaptation to the hyperosmolality in the renal medulla by promoting expression of its target genes.

His current research is directed in two areas. 1. Molecular mechanism of tonicity sensing by TonEBP in the context of nuclear translocation and post-translational modifications by SUMO (small ubiquitin-modifiers) and acetylation; and 2. Physiological and pathological function of TonEBP in diabetic nephropathy, blood pressure regulation and stress resistance.

Heddwen Brooks

Heddwen Brooks earned her PhD from Imperial College, University of London. For her post-doctoral fellowship she came to the University of Arizona to work on aquaporins. She followed this with a fellowship at the Laboratory of Kidney and Electrolyte Metabolism, before becoming an Assistant Professor in the Department of Physiology, at the University of Arizona in 2001, and was promoted to Associate Professor in 2008. In 2007 she received the American Physiological Society Lazaro J. Mandel Young Investigator Award; and in 2009 she received the Renal Young Investigator Award at the annual meeting of the Federation of American Societies for Experimental Biology.

The focus of her research is the hormonal regulation of renal function, focusing on the role that vasopressin and the collecting duct plays in fluid homeostasis. Brooks is best known for her development of microarray technology to address in vivo signaling pathways involved in the hormonal regulation of renal function. Aquaporin (AQP) 1 knockout mice have a defect in the renal concentrating gradient because of their inability to generate a hyperosmotic medullary interstitium. To determine the effect of vasopressin on renal medullary function and to identify novel signaling pathways in the absence of high local osmolarity AQP1KO mice were used for microarray studies. Several novel candidates of vasopressin regulation have been identified.

More recently the Brooks lab has been pursuing the role of steroid hormones in the development of diabetic kidney damage. Perimenopause, the 5-10 years preceding menopause in women, is increasingly recognized as a critical period in the development and treatment of many diseases. The 4-vinylcyclohexene diepoxide model of menopause progresses gradually through perimenopause to post-menopause and preserves the postmenopausal ovarian production of androgens. Using this model in combination with a type 1 model of diabetes the Brooks lab recently demonstrated that changes in renal structure and function associated with diabetic kidney disease occurred more rapidly in the post-menopause kidney than in cycling controls.

She has been very active in the American Physiological Society, she is a member of the APS Renal Steering Section, has served as chair of the renal awards committee, has served on the APS Nominating Committee, and is currently on the APS Committee of Committees. She is on the Editorial Board of the American Journal of Physiology-Renal Physiology, and is an invited editor for the 23rd edition of the late William Ganong’s well-known Review in Medical Physiology.

Daniel Markovich

Daniel Markovich is a Professor of Physiology in the School of Biomedical Sciences of the University of Queensland, Brisbane, Australia. His research interests are in the study of the physiology, pathophysiology and regulation of mammalian ion transporters, involved in mediating transcellular movement of ions (sulfate, chloride, phosphate) across epithelial cells of the kidney, small intestine, liver and brain. His lab has cloned and characterized several ion transporters and recently generated transporter null mice, in order to determine their physiological roles in the body.

Philip Poronnik

Philip Poronnik is Professor in the RMIT University, Australia. His research interests are in the molecular physiology of epithelial ion transport: changes in membrane transport that occur in the kidney in diabetes mellitus. His research aims at characterising the molecular mechanisms that regulate albumin uptake by the proximal tubule of the kidney and establishing the relationship between albumin uptake and sodium retention.

Glenda Gobe

Associate Professor Glenda Gobe is known internationally as a molecular pathology expert specialising in the role of apoptosis in kidney disease. She is a Director of the Centre for Kidney Disease Research, School of Medicine, University of Queensland. She has overseas training from the College of Physicians and Surgeons, Columbia University with Professor Ralph Buttyan, one of the leading world experts in the molecular biology of apoptosis and specialising in prostate cancer research. Her research also promotes the understanding of the role of apoptosis in cancer biology and general disease. Her current research focuses on the role and modulation of oxidative stress and mitochondrial dysfunction in renal disease, including chronic kidney disease and renal cancer. Glenda Gobe is the author of over 120 original research articles, reviews and book chapters. She lectures in molecular pathobiology at the Schools of Medicine, Biomedical Sciences and Chemistry and Microbial Sciences, University of Queensland, and the School of Biomolecular and Physical Sciences at Griffith University. She has supervised 19 students to successful completion of PhD, MSc, MMedSc, and Honours enrolments.

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